Cellular ageing is the progressive decline in cellular function and viability caused by genetic abnormalities and the accumulation of damage over time. There are several theories that attempt to explain the aging process, including evolutionary, molecular, cellular, and systemic theories. At the cellular level, ageing is caused by DNA damage from both endogenous and exogenous sources, as well as telomere shortening after each cell division. Other factors that contribute to cellular ageing include defective protein homeostasis, disrupted nutrient sensing pathways, and a decline in cellular repair mechanisms. Premature ageing disorders provide insights into how disrupting certain ageing processes can accelerate ageing. While cellular senescence limits cell proliferation and acts as a tumor suppressor, it is
Describes the process of ageing in cells, factors affecting cells like telomere, free radicals, oxidative stress, DNA damage, environmental factors, proteostasis, mitochondrial disfunction etc are described
1. Cellular aging results from a progressive decline in the proliferative capacity and lifespan of cells due to accumulation of damage from genetic and environmental factors over time.
2. Key mechanisms of cellular aging include shortening of telomeres, accumulation of aging pigments, free radicals, and changes in gene expression through epigenetic alterations.
3. Apoptosis is a tightly regulated form of programmed cell death where cells activate enzymes to degrade their own nuclear DNA and proteins, then break into fragments that are cleared by phagocytes before potential inflammation from secondary necrosis.
- Aging is characterized by a declining ability to respond to stress, increasing homeostatic imbalance, and higher risk of disease. It is a degenerative process with no positive features.
- The main factors that act in the aging process include mitochondrial dysfunction, DNA damage and repair, cell cycle regulation, telomere shortening, and changes in transcription and translation.
- Theories of aging include the molecular gene theory, cellular theories involving free radicals and apoptosis, and evolutionary theories such as antagonistic pleiotropy and mutation accumulation. Apoptosis is programmed cell death while necrosis is unregulated cell death from external factors like toxins.
Apoptosis is a natural and programmed form of cell death that occurs in multicellular organisms. It was first described in 1842 and distinguished from necrosis in 1965. During apoptosis, a series of biochemical events lead to changes in the cell and its death, allowing it to be eliminated in a controlled way that does not cause inflammation. This process is regulated by complex signaling pathways within the cell and involves mitochondria, caspases and other components. Defects in apoptosis can result in cancer if cell death is inhibited or neurodegenerative diseases if cell death is excessive.
Apoptosis is a tightly regulated process of programmed cell death that removes unnecessary or damaged cells. It is mediated by caspases, cysteine-dependent aspartate-directed proteases, that cleave key cellular proteins and lead to cell death. Apoptosis occurs through the intrinsic mitochondrial pathway or the extrinsic death receptor pathway and plays an important role in development, tissue homeostasis, and defense against infection and cancer. Defects in apoptosis can lead to neurodegenerative diseases, autoimmunity, and cancer.
Apoptosis, or programmed cell death, is an important physiological process that eliminates unwanted or damaged cells. There are two main pathways that trigger apoptosis - the extrinsic or death receptor pathway, and the intrinsic or mitochondrial pathway. The extrinsic pathway involves death receptors and ligands that activate caspase enzymes. The intrinsic pathway occurs in response to cellular stress and involves mitochondrial outer membrane permeabilization and the release of proteins like cytochrome c. This forms the apoptosome complex and activates caspase-9 and caspase-3, leading to apoptosis. Apoptosis is a highly regulated process involving Bcl-2 family proteins, caspase enzymes, and characteristic morphological changes including cell shrinkage, nuclear fragmentation, and membrane blebbing. Assays to detect
Apoptosis also known as cell suicide. Difference between necrosis and apoptosis. Changes in apoptosis. Mechanism of apoptosis. Functional significance of apoptosis. Applied aspects of apoptosis
Describes the process of ageing in cells, factors affecting cells like telomere, free radicals, oxidative stress, DNA damage, environmental factors, proteostasis, mitochondrial disfunction etc are described
1. Cellular aging results from a progressive decline in the proliferative capacity and lifespan of cells due to accumulation of damage from genetic and environmental factors over time.
2. Key mechanisms of cellular aging include shortening of telomeres, accumulation of aging pigments, free radicals, and changes in gene expression through epigenetic alterations.
3. Apoptosis is a tightly regulated form of programmed cell death where cells activate enzymes to degrade their own nuclear DNA and proteins, then break into fragments that are cleared by phagocytes before potential inflammation from secondary necrosis.
- Aging is characterized by a declining ability to respond to stress, increasing homeostatic imbalance, and higher risk of disease. It is a degenerative process with no positive features.
- The main factors that act in the aging process include mitochondrial dysfunction, DNA damage and repair, cell cycle regulation, telomere shortening, and changes in transcription and translation.
- Theories of aging include the molecular gene theory, cellular theories involving free radicals and apoptosis, and evolutionary theories such as antagonistic pleiotropy and mutation accumulation. Apoptosis is programmed cell death while necrosis is unregulated cell death from external factors like toxins.
Apoptosis is a natural and programmed form of cell death that occurs in multicellular organisms. It was first described in 1842 and distinguished from necrosis in 1965. During apoptosis, a series of biochemical events lead to changes in the cell and its death, allowing it to be eliminated in a controlled way that does not cause inflammation. This process is regulated by complex signaling pathways within the cell and involves mitochondria, caspases and other components. Defects in apoptosis can result in cancer if cell death is inhibited or neurodegenerative diseases if cell death is excessive.
Apoptosis is a tightly regulated process of programmed cell death that removes unnecessary or damaged cells. It is mediated by caspases, cysteine-dependent aspartate-directed proteases, that cleave key cellular proteins and lead to cell death. Apoptosis occurs through the intrinsic mitochondrial pathway or the extrinsic death receptor pathway and plays an important role in development, tissue homeostasis, and defense against infection and cancer. Defects in apoptosis can lead to neurodegenerative diseases, autoimmunity, and cancer.
Apoptosis, or programmed cell death, is an important physiological process that eliminates unwanted or damaged cells. There are two main pathways that trigger apoptosis - the extrinsic or death receptor pathway, and the intrinsic or mitochondrial pathway. The extrinsic pathway involves death receptors and ligands that activate caspase enzymes. The intrinsic pathway occurs in response to cellular stress and involves mitochondrial outer membrane permeabilization and the release of proteins like cytochrome c. This forms the apoptosome complex and activates caspase-9 and caspase-3, leading to apoptosis. Apoptosis is a highly regulated process involving Bcl-2 family proteins, caspase enzymes, and characteristic morphological changes including cell shrinkage, nuclear fragmentation, and membrane blebbing. Assays to detect
Apoptosis also known as cell suicide. Difference between necrosis and apoptosis. Changes in apoptosis. Mechanism of apoptosis. Functional significance of apoptosis. Applied aspects of apoptosis
1. Apoptosis is a tightly regulated process of programmed cell death that removes unwanted or damaged cells. It involves activation of caspases and degradation of nuclear DNA and proteins.
2. There are two main pathways that initiate apoptosis - the extrinsic pathway which involves death receptors, and the intrinsic pathway which involves the mitochondria. Both pathways activate caspases that execute the cell death program.
3. Disorders of apoptosis can result in disease states like cancer if cells fail to undergo apoptosis in response to damage, or neurodegeneration if excessive apoptosis occurs. A delicate balance of pro-apoptotic and anti-apoptotic proteins regulates apoptosis.
This document discusses cellular aging and theories of aging. It covers several key points:
1) Cellular senescence and the Hayflick limit, where cells stop dividing after a certain number of divisions.
2) Theories of aging including the free radical theory, somatic mutation theory, and telomere loss theory.
3) Types of cell death including apoptosis, necrosis, necroptosis, and pyroptosis. Programmed cell death limits inflammation while necrosis causes damage and inflammation.
Apoptosis, also known as programmed cell death, is a natural process by which cells self-destruct in response to internal or external signals. It is distinct from necrosis in that it involves chromatin condensation, cell shrinkage, and preservation of organelles, allowing for rapid engulfment by neighboring cells without inflammation. Apoptosis is initiated through either the intrinsic mitochondrial pathway or the extrinsic death receptor pathway and is executed by caspases, a family of cysteine proteases. It plays an essential role in development and homeostasis by removing damaged or unneeded cells.
Cell and tissue regeneration involves cell proliferation driven by growth factors and the development of mature cells from stem cells. There are three types of tissues based on their proliferative capacity: labile tissues which continuously divide, stable tissues which have limited proliferation, and permanent tissues which do not regenerate. Liver regeneration is remarkable, with up to 90% resection compensated by hepatocyte proliferation induced by cytokines and growth factors. When hepatocytes are impaired, liver progenitor cells contribute to repopulation.
The document discusses apoptosis (programmed cell death) through three parts:
1) An introduction to apoptosis, its history, and how it is important in development and physiology.
2) The mechanisms and pathways of apoptosis, including caspases, the intrinsic mitochondrial pathway, extrinsic death receptor pathway, and Bcl-2 family of proteins.
3) The importance of apoptosis in normal development and physiology through tissue sculpting, but that defects can lead to diseases like cancer, autoimmunity, and neurodegeneration when there is too much or too little apoptosis.
Aging is characterized by a declining ability to respond to stress and increased risk of disease. Differences in maximum lifespan between species correspond to different rates of aging, affected by genetic factors. Cells lose the ability to divide and function through the process of senescence. Traditional theories of aging include programmed and stochastic theories. More recent theories include molecular, cellular, and system-level theories. The free radical theory proposes that oxidative damage from free radicals produced during metabolism accumulates over time and causes aging. Telomere shortening leads to cell senescence.
Apoptosis is a process of programmed cell death that occurs in multicellular organisms. Biochemical events lead to characteristic cell changes (morphology) and death.
General pathology lecture 4 cellular adaptationLheanne Tesoro
Cellular adaptations can occur through hyperplasia, hypertrophy, atrophy, or metaplasia in response to stress or changes in workload or stimulation. Hyperplasia involves an increased number of cells through cell proliferation. Hypertrophy involves cellular enlargement without an increase in cell number. Atrophy is a decrease in cell size. Metaplasia is the replacement of one adult cell type with another. Examples provided include uterine hyperplasia during pregnancy, cardiac hypertrophy in hypertension, muscle fiber atrophy after injury or disuse, and squamous metaplasia in the lungs of smokers. Dysplasia refers to alterations in cell size, shape, and organization and is a pre-cancerous condition.
Difference between Apoptosis versus Necrosis and Types of Necrosis.pptxRukhshanda Ramzaan
Apoptosis Versus Nercosis
Apoptosis Necrosis
Predefined cell suicide or programmed cell death. Natural physiological Process. Involve one cell at a time. Cell shrinkage (Dense eosinophilic cytoplasm) Pyknosis (Condensation) and Karyorrhexis (fragmentation) of nuclear material Formation of membrane blebs and apoptotic bodies
Phagocytosis of apoptotic bodies by Macrophages
Caspase dependent pathway
No Inflammation (no immune response) Premature, unprogrammed cell death always pathological. Involve many cells Cell Swelling (Swelling of endoplasmic reticulum and mitochondria) and membrane blebs Pyknosis (condensation), Karyorrhexis (Fragmentation) and Karyolysis (lysis)of the nucleus. Breakdown of the plasma membrane, organelles (enzymatic digestion), leakage of cellular contents
Increased eosinophilia, Accumulation of Myelin figures (whorled precipitated Phospholipids)
Initiate Inflammation (Strong immune response)
1. Apoptosis is a tightly regulated process of programmed cell death that involves the activation of caspases and degradation of nuclear and cellular components.
2. It can be triggered through intrinsic mitochondrial pathways or extrinsic death receptor pathways and plays an important physiological role in development, immune system maturation, and maintenance of tissue homeostasis.
3. Dysregulation of apoptosis can contribute to cancer, autoimmune diseases, and neurodegenerative disorders by allowing cells to survive inappropriately or undergo excessive cell death.
1) Apoptosis is a process of programmed cell death that is important for normal development and physiology, as it helps remove excess, damaged, or dangerous cells.
2) It occurs through intrinsic and extrinsic pathways that involve caspase proteases and results in characteristic cell changes like blebbing and nuclear fragmentation.
3) Between 50-70 billion cells die per day in humans due to apoptosis, which is critical for processes like immune system maturation and tissue remodeling.
The document summarizes key aspects of apoptosis including:
- The origins and definition of the term apoptosis from Greek meaning "falling leaves".
- The significance of apoptosis in development and maintenance of tissues by removing excess or damaged cells.
- The morphological features of apoptosis including membrane blebbing, nuclear fragmentation, and formation of apoptotic bodies.
- The molecular mechanisms including caspase signaling pathways like the intrinsic pathway involving mitochondria and the extrinsic pathway involving death receptors.
- Regulatory mechanisms involving proteins like Bcl-2 that balance survival and death signals.
- Dysregulation of apoptosis can lead to diseases like cancer, autoimmune disorders, and HIV infection.
This document discusses cellular injury. It defines cell injury as changes to a cell's internal and external environment caused by various stresses from etiological agents. Short term, mild stresses can lead to reversible cell injury through adaptations, while long term, severe stresses can cause irreversible injury and cell death. Reversible injury involves things like decreased ATP and protein synthesis, while irreversible injury includes nuclear damage, lysosomal enzyme release, and cell digestion. The document outlines various causes of cell injury and the morphological changes seen in reversible versus irreversible injury states.
This document summarizes the molecular mechanisms of cancer metastasis. It begins with an overview of metastasis and defines it as the process by which tumor cells spread from the primary site to distant organs via the circulatory system. It then discusses the major steps in metastasis, including invasion, intravasation, survival in circulation, arrest at secondary sites, and extravasation. The key molecular components that drive metastasis are matrix-degrading enzymes like MMPs, cell adhesion molecules like integrins and E-cadherin, and cytoskeletal regulators like Rho GTPases that control cell motility. Signaling pathways activated by HGF/c-Met and other motility factors also promote invasion and metastasis. Understanding the molecular underpinnings of
This document summarizes key concepts about neoplasms and cancer. It defines neoplasms as abnormal masses of tissue with uncontrolled growth. Oncology is the study of tumors. Tumors can be benign, meaning localized growth, or malignant (cancerous), meaning they can invade other tissues and metastasize. Cancers arise from genetic changes in cells that disrupt normal growth regulation. Key cancer genes include oncogenes that promote growth and tumor suppressor genes that inhibit growth. Evasion of apoptosis and unlimited replication are also critical to cancer development.
The document discusses programmed cell death or apoptosis. It begins by defining apoptosis as a regulated process where cells self-degrade to eliminate unwanted or damaged cells. Between 50-70 billion cells die daily in humans through apoptosis. The document then covers the history of apoptosis research and discovery. It discusses the role of caspases as executioners of apoptosis and the intrinsic and extrinsic pathways. Conditions where apoptosis is increased or decreased are examined, along with potential therapeutic targets like caspase inhibitors.
IMMUNE RESPONSE TO TUMORS-Humoral immunity
-Cellular Immunity- Failure of Host Defenses
- Evasion of Immune Responses by Tumors
- Cancer Immunosurveillance vs Immunoediting- Immunotherapy
This document provides an overview of cell injury and cell death processes presented by Dr. Marc Imhotep Cray. It discusses reversible cell injury mechanisms including hydropic swelling, intracellular accumulations, and cellular adaptation processes. It also covers irreversible cell injury mechanisms of necrosis and apoptosis. Necrosis types such as coagulative, liquefactive, caseous, and fat necrosis are described. The document provides histological images and discusses the cellular and molecular mechanisms involved in different types of cell injury and death.
This document discusses tissue repair and regeneration. It notes that tissue repair refers to restoring tissue architecture and function after injury through regeneration via residual cell proliferation or connective tissue deposition and scarring. The key aspects of regeneration are cell proliferation driven by growth factors and stem cell differentiation. Connective tissue deposition and scarring occurs when tissues cannot regenerate fully and lay down collagen fibers. The liver has remarkable regenerative abilities through hepatocyte proliferation and progenitor cells.
Chemical carcinogenesis involves chemicals being metabolized in vivo into electrophilic reactants that can damage DNA. Carcinogenesis is a multi-stage process involving initiation, promotion, and progression. Initiation involves acquiring genetic changes that put a cell on a cancer path. Promotion provides a selective advantage allowing primed cells to survive locally. Progression accumulates further changes for malignancy. Chronic inflammation contributes at each stage by generating DNA-damaging species and altering cell-stroma relationships to facilitate invasion and spread. The most common chemical carcinogens metabolize into electrophilic reactants that can damage DNA.
This document discusses several theories of aging at the cellular, molecular, evolutionary, and systems levels. The main cellular theories discussed are telomere shortening and free radical damage accumulation over time. Evolutionary theories proposed include mutation accumulation, antagonistic pleiotropy, and the declining force of natural selection with age. Lifestyle and future biomedical interventions are mentioned as potential ways to promote healthy aging or extend lifespan.
This presentation provides an overview of Cell senescence, Aging, Theories of Aging,principle of senescence, Mechanism of action, Factors, Diseases caused due to this action, Senescence and cancer, Insulin signalling cascade, Telomere shortening.
1. Apoptosis is a tightly regulated process of programmed cell death that removes unwanted or damaged cells. It involves activation of caspases and degradation of nuclear DNA and proteins.
2. There are two main pathways that initiate apoptosis - the extrinsic pathway which involves death receptors, and the intrinsic pathway which involves the mitochondria. Both pathways activate caspases that execute the cell death program.
3. Disorders of apoptosis can result in disease states like cancer if cells fail to undergo apoptosis in response to damage, or neurodegeneration if excessive apoptosis occurs. A delicate balance of pro-apoptotic and anti-apoptotic proteins regulates apoptosis.
This document discusses cellular aging and theories of aging. It covers several key points:
1) Cellular senescence and the Hayflick limit, where cells stop dividing after a certain number of divisions.
2) Theories of aging including the free radical theory, somatic mutation theory, and telomere loss theory.
3) Types of cell death including apoptosis, necrosis, necroptosis, and pyroptosis. Programmed cell death limits inflammation while necrosis causes damage and inflammation.
Apoptosis, also known as programmed cell death, is a natural process by which cells self-destruct in response to internal or external signals. It is distinct from necrosis in that it involves chromatin condensation, cell shrinkage, and preservation of organelles, allowing for rapid engulfment by neighboring cells without inflammation. Apoptosis is initiated through either the intrinsic mitochondrial pathway or the extrinsic death receptor pathway and is executed by caspases, a family of cysteine proteases. It plays an essential role in development and homeostasis by removing damaged or unneeded cells.
Cell and tissue regeneration involves cell proliferation driven by growth factors and the development of mature cells from stem cells. There are three types of tissues based on their proliferative capacity: labile tissues which continuously divide, stable tissues which have limited proliferation, and permanent tissues which do not regenerate. Liver regeneration is remarkable, with up to 90% resection compensated by hepatocyte proliferation induced by cytokines and growth factors. When hepatocytes are impaired, liver progenitor cells contribute to repopulation.
The document discusses apoptosis (programmed cell death) through three parts:
1) An introduction to apoptosis, its history, and how it is important in development and physiology.
2) The mechanisms and pathways of apoptosis, including caspases, the intrinsic mitochondrial pathway, extrinsic death receptor pathway, and Bcl-2 family of proteins.
3) The importance of apoptosis in normal development and physiology through tissue sculpting, but that defects can lead to diseases like cancer, autoimmunity, and neurodegeneration when there is too much or too little apoptosis.
Aging is characterized by a declining ability to respond to stress and increased risk of disease. Differences in maximum lifespan between species correspond to different rates of aging, affected by genetic factors. Cells lose the ability to divide and function through the process of senescence. Traditional theories of aging include programmed and stochastic theories. More recent theories include molecular, cellular, and system-level theories. The free radical theory proposes that oxidative damage from free radicals produced during metabolism accumulates over time and causes aging. Telomere shortening leads to cell senescence.
Apoptosis is a process of programmed cell death that occurs in multicellular organisms. Biochemical events lead to characteristic cell changes (morphology) and death.
General pathology lecture 4 cellular adaptationLheanne Tesoro
Cellular adaptations can occur through hyperplasia, hypertrophy, atrophy, or metaplasia in response to stress or changes in workload or stimulation. Hyperplasia involves an increased number of cells through cell proliferation. Hypertrophy involves cellular enlargement without an increase in cell number. Atrophy is a decrease in cell size. Metaplasia is the replacement of one adult cell type with another. Examples provided include uterine hyperplasia during pregnancy, cardiac hypertrophy in hypertension, muscle fiber atrophy after injury or disuse, and squamous metaplasia in the lungs of smokers. Dysplasia refers to alterations in cell size, shape, and organization and is a pre-cancerous condition.
Difference between Apoptosis versus Necrosis and Types of Necrosis.pptxRukhshanda Ramzaan
Apoptosis Versus Nercosis
Apoptosis Necrosis
Predefined cell suicide or programmed cell death. Natural physiological Process. Involve one cell at a time. Cell shrinkage (Dense eosinophilic cytoplasm) Pyknosis (Condensation) and Karyorrhexis (fragmentation) of nuclear material Formation of membrane blebs and apoptotic bodies
Phagocytosis of apoptotic bodies by Macrophages
Caspase dependent pathway
No Inflammation (no immune response) Premature, unprogrammed cell death always pathological. Involve many cells Cell Swelling (Swelling of endoplasmic reticulum and mitochondria) and membrane blebs Pyknosis (condensation), Karyorrhexis (Fragmentation) and Karyolysis (lysis)of the nucleus. Breakdown of the plasma membrane, organelles (enzymatic digestion), leakage of cellular contents
Increased eosinophilia, Accumulation of Myelin figures (whorled precipitated Phospholipids)
Initiate Inflammation (Strong immune response)
1. Apoptosis is a tightly regulated process of programmed cell death that involves the activation of caspases and degradation of nuclear and cellular components.
2. It can be triggered through intrinsic mitochondrial pathways or extrinsic death receptor pathways and plays an important physiological role in development, immune system maturation, and maintenance of tissue homeostasis.
3. Dysregulation of apoptosis can contribute to cancer, autoimmune diseases, and neurodegenerative disorders by allowing cells to survive inappropriately or undergo excessive cell death.
1) Apoptosis is a process of programmed cell death that is important for normal development and physiology, as it helps remove excess, damaged, or dangerous cells.
2) It occurs through intrinsic and extrinsic pathways that involve caspase proteases and results in characteristic cell changes like blebbing and nuclear fragmentation.
3) Between 50-70 billion cells die per day in humans due to apoptosis, which is critical for processes like immune system maturation and tissue remodeling.
The document summarizes key aspects of apoptosis including:
- The origins and definition of the term apoptosis from Greek meaning "falling leaves".
- The significance of apoptosis in development and maintenance of tissues by removing excess or damaged cells.
- The morphological features of apoptosis including membrane blebbing, nuclear fragmentation, and formation of apoptotic bodies.
- The molecular mechanisms including caspase signaling pathways like the intrinsic pathway involving mitochondria and the extrinsic pathway involving death receptors.
- Regulatory mechanisms involving proteins like Bcl-2 that balance survival and death signals.
- Dysregulation of apoptosis can lead to diseases like cancer, autoimmune disorders, and HIV infection.
This document discusses cellular injury. It defines cell injury as changes to a cell's internal and external environment caused by various stresses from etiological agents. Short term, mild stresses can lead to reversible cell injury through adaptations, while long term, severe stresses can cause irreversible injury and cell death. Reversible injury involves things like decreased ATP and protein synthesis, while irreversible injury includes nuclear damage, lysosomal enzyme release, and cell digestion. The document outlines various causes of cell injury and the morphological changes seen in reversible versus irreversible injury states.
This document summarizes the molecular mechanisms of cancer metastasis. It begins with an overview of metastasis and defines it as the process by which tumor cells spread from the primary site to distant organs via the circulatory system. It then discusses the major steps in metastasis, including invasion, intravasation, survival in circulation, arrest at secondary sites, and extravasation. The key molecular components that drive metastasis are matrix-degrading enzymes like MMPs, cell adhesion molecules like integrins and E-cadherin, and cytoskeletal regulators like Rho GTPases that control cell motility. Signaling pathways activated by HGF/c-Met and other motility factors also promote invasion and metastasis. Understanding the molecular underpinnings of
This document summarizes key concepts about neoplasms and cancer. It defines neoplasms as abnormal masses of tissue with uncontrolled growth. Oncology is the study of tumors. Tumors can be benign, meaning localized growth, or malignant (cancerous), meaning they can invade other tissues and metastasize. Cancers arise from genetic changes in cells that disrupt normal growth regulation. Key cancer genes include oncogenes that promote growth and tumor suppressor genes that inhibit growth. Evasion of apoptosis and unlimited replication are also critical to cancer development.
The document discusses programmed cell death or apoptosis. It begins by defining apoptosis as a regulated process where cells self-degrade to eliminate unwanted or damaged cells. Between 50-70 billion cells die daily in humans through apoptosis. The document then covers the history of apoptosis research and discovery. It discusses the role of caspases as executioners of apoptosis and the intrinsic and extrinsic pathways. Conditions where apoptosis is increased or decreased are examined, along with potential therapeutic targets like caspase inhibitors.
IMMUNE RESPONSE TO TUMORS-Humoral immunity
-Cellular Immunity- Failure of Host Defenses
- Evasion of Immune Responses by Tumors
- Cancer Immunosurveillance vs Immunoediting- Immunotherapy
This document provides an overview of cell injury and cell death processes presented by Dr. Marc Imhotep Cray. It discusses reversible cell injury mechanisms including hydropic swelling, intracellular accumulations, and cellular adaptation processes. It also covers irreversible cell injury mechanisms of necrosis and apoptosis. Necrosis types such as coagulative, liquefactive, caseous, and fat necrosis are described. The document provides histological images and discusses the cellular and molecular mechanisms involved in different types of cell injury and death.
This document discusses tissue repair and regeneration. It notes that tissue repair refers to restoring tissue architecture and function after injury through regeneration via residual cell proliferation or connective tissue deposition and scarring. The key aspects of regeneration are cell proliferation driven by growth factors and stem cell differentiation. Connective tissue deposition and scarring occurs when tissues cannot regenerate fully and lay down collagen fibers. The liver has remarkable regenerative abilities through hepatocyte proliferation and progenitor cells.
Chemical carcinogenesis involves chemicals being metabolized in vivo into electrophilic reactants that can damage DNA. Carcinogenesis is a multi-stage process involving initiation, promotion, and progression. Initiation involves acquiring genetic changes that put a cell on a cancer path. Promotion provides a selective advantage allowing primed cells to survive locally. Progression accumulates further changes for malignancy. Chronic inflammation contributes at each stage by generating DNA-damaging species and altering cell-stroma relationships to facilitate invasion and spread. The most common chemical carcinogens metabolize into electrophilic reactants that can damage DNA.
This document discusses several theories of aging at the cellular, molecular, evolutionary, and systems levels. The main cellular theories discussed are telomere shortening and free radical damage accumulation over time. Evolutionary theories proposed include mutation accumulation, antagonistic pleiotropy, and the declining force of natural selection with age. Lifestyle and future biomedical interventions are mentioned as potential ways to promote healthy aging or extend lifespan.
This presentation provides an overview of Cell senescence, Aging, Theories of Aging,principle of senescence, Mechanism of action, Factors, Diseases caused due to this action, Senescence and cancer, Insulin signalling cascade, Telomere shortening.
This document discusses the molecular basis of aging and longevity. It covers several topics: genes and aging pathways like DNA repair and insulin signaling; environmental and epigenetic factors such as oxidative damage, diet, and calorie restriction; and promoting longevity. Key points include conserved genetic pathways regulating aging across species, the role of genes encoding DNA repair enzymes and insulin signaling proteins, and how calorie restriction and reducing insulin/IGF-1 signaling can increase longevity in various organisms.
Aging is a progressive accumulation of changes over time that increases susceptibility to disease and death. It results from the gradual deterioration of molecular and cellular components and physiological systems. The main theories of aging include DNA damage accumulation through reactive oxygen species and reduced DNA repair, telomere shortening limiting cell division, disrupted nutrient sensing pathways involving insulin/IGF-1 signaling and mTOR, and impaired chromatin remodeling and DNA repair by sirtuins. Interventions that reduce oxidative stress, caloric intake, insulin/IGF-1 signaling, and mTOR activation can help delay the aging process and extend lifespan in various model organisms.
This document discusses the biology of healthy aging and longevity. It covers several topics:
1) Molecular mechanisms of aging including genome integrity, telomeres, epigenetics, protein stability, and pathways like mTOR, IIS, AMPK, and sirtuins that modify aging.
2) Biological models like yeast, worms, flies and mice that are used to study aging mechanisms.
3) Calorie restriction which increases longevity across species by reversing signs of aging.
4) Maintaining genome, telomere and epigenome integrity is important for healthy aging and preventing diseases.
5) Environmental factors and nutrition influence aging through epigenetic changes.
This document discusses aging and the aging kidney. It begins by outlining the epidemiology and theories of aging, including how aging is a cumulative process influenced by both genetic and environmental factors. It then examines age-related changes in the kidney, including morphological changes like glomerulosclerosis, interstitial fibrosis, and vascular sclerosis. These changes are thought to be caused by factors like telomere shortening, oxidative stress, inflammation, and accumulation of advanced glycation end products over time. Managing these age-related changes and underlying disease processes is an important part of caring for the growing elderly population.
Ageing is caused by the progressive loss of structural and functional capacity in cells over time, leading to death. It is influenced 60% by genetic factors and 40% by environmental factors such as trauma, disease, diet, and stress. The main structural and biochemical changes that occur during ageing include the accumulation of oxidative damage in cells from reactive oxygen species, advanced glycation end products, and abnormally folded proteins. Telomerase plays a role in preventing shortening of telomeres during cell division. Restricting calorie intake and maintaining good health habits can help delay the cellular ageing process.
Ageing is a progressive accumulation of changes over time that leads to deterioration of structure and function. It increases susceptibility to diseases and mortality. There are three main types of ageing: primary, secondary, and tertiary. Several theories attempt to explain the biological process of ageing, including programmed ageing, telomere shortening, mitochondrial dysfunction, and stem cell exhaustion. The body undergoes numerous changes with ageing including loss of bone and muscle mass, stiffening of arteries and lungs, greying of hair, thinning skin, and cognitive decline.
Cell aging is characterized by a declining ability to respond to stress and increased homeostatic imbalance. Aging theories include programmed and stochastic theories. More recently, theories are categorized as molecular, cellular, and system-level. The free radical theory of aging proposes that reactive oxygen species generated during metabolism cause cumulative oxidative damage, resulting in structural degeneration, apoptosis, functional decline, and age-related diseases. Some believe oxidative stress is the predominant cause of age-associated degenerative changes. Telomere shortening causes cell senescence as telomeres reach a critical length after repeated cell division.
This document discusses several key physiological traits associated with aging:
Genomic instability causes accumulation of genetic damage to DNA over a lifetime from various sources. Telomere attrition refers to shortening of telomeres each time a cell divides, ultimately limiting it to around 50 divisions. Epigenetic alterations change gene expression through factors like histone modifications and chromatin structure. Loss of proteostasis reduces the cell's ability to regulate protein production, allowing damaged proteins to accumulate. Additional traits discussed include mitochondrial dysfunction, deregulated nutrient sensing, altered intercellular communication, and cellular senescence.
This document discusses 15 major theories on the biological basis of aging:
1) Evolutionary theories propose that lifespan is genetically determined and subject to natural selection.
2) The telomere theory suggests that shortening telomeres act as a "clock" that limits the number of times a cell can divide.
3) The reproductive-cell cycle theory links aging to declining reproductive hormones that dysregulate cell signaling.
4) DNA damage theories posit that aging results from accumulated DNA damage over time.
5) The gene loss theory observes that aging involves the gradual loss of genes, particularly in mitochondria.
The document summarizes cellular adaptation and injury. It states that cells can undergo adaptation to achieve a new steady state and preserve viability when faced with physiological stresses, but severe or persistent stress can lead to reversible or irreversible injury. It describes different types of cellular adaptation like atrophy, hypertrophy, hyperplasia and metaplasia. It also discusses various causes of cellular injury like hypoxia, chemicals, infections and genetic factors. The key mechanisms of injury involve defects in membranes, ATP production and protein/DNA integrity.
The document discusses senescence and aging at the cellular, organismal, and population levels. At the cellular level, senescence refers to a cell losing its ability to divide over time due to factors like telomere shortening and oxidative damage. Organismal senescence is characterized by a decline in fertility and increased mortality risk with age. Population studies of senescence examine age-specific survival and mortality rates using life tables to analyze factors influencing life history strategies. The genetic basis of senescence is complex, with multiple genes and environmental influences contributing to the aging process.
Cellular aging is regulated by genes and results from the accumulation of genetic abnormalities and molecular damage over time. It leads to a progressive decline in cellular function and viability. Several mechanisms contribute to cellular aging, including DNA damage from environmental factors that is not fully repaired, telomere shortening after each cell division in the absence of telomerase, and impaired protein folding and degradation. Studies in model organisms have identified conserved genetic pathways and processes that influence the aging process.
Theories of Aging - Part 1 in medicine and health sciencesJackTan88
This document provides an overview of theories of aging. It discusses both biological/physiological and psychological perspectives on aging. From a biological standpoint, it describes programmed aging theories like the telomere theory, which proposes that cells can only divide a finite number of times due to shortening telomeres. It also discusses error theories of aging, like the free radical theory, which suggests aging results from cellular damage over time. The document aims to explain the aging process and major theories about what causes aging.
Apoptosis, or programmed cell death, is essential for development and survival. It involves the activation of enzymes that dissolve nuclear and cytoplasmic components. Dysregulation of apoptosis can lead to cancer. There are three main mechanisms by which cancer cells acquire resistance to apoptosis: 1) disruption of the balance between pro-apoptotic and anti-apoptotic proteins, 2) reduction in caspase function, and 3) impaired death receptor signaling. Mutation or inactivation of the p53 tumor suppressor gene, which regulates apoptosis, frequently occurs in cancer through various mechanisms like HPV infection, MDM2 amplification, AKT alterations, and PTEN mutations.
cell adaptation and cell injury - Copy-4 copy.pptxNadiirMahamoud
Cells respond to stress through adaptation, injury, and death. As stress exceeds adaptive responses, injury develops and can lead to reversible or irreversible cell death. Key targets of injury include ATP depletion, damage to cell membranes through increased calcium levels, and damage to mitochondria and lysosomes. Membrane damage can trigger cell death through apoptosis or necrosis depending on severity. Understanding cellular responses to stress is crucial for evolving disease.
The document discusses normal aging and provides definitions and theories related to the aging process. It addresses topics like the mechanisms of aging, theories of aging, hallmarks of aging, and changes that occur in the brain with aging. It also discusses mental health and personality in older adults, coping strategies, and factors involved in successful aging. The document provides an overview of many aspects of the normal aging process from a biological, psychological, and social perspective.
Cellular aging signalling and transcriptional pathways-2018dr_ekbalabohashem
This document discusses several cellular pathways involved in aging and stress responses, including the heat shock response, ubiquitin-proteasome system, organelle-specific pathways in the endoplasmic reticulum, mitochondria, and lysosome/autophagy. It describes how these pathways degrade damaged proteins and clear cellular waste, but their function declines with age, leading to accumulation of damage that contributes to age-related diseases. Maintaining the function of these stress response pathways through mild stresses or dietary interventions can promote healthy aging.
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
2. What is Ageing
Aging is the result of the progressive and irreversible decline of the
capacity of an organism to adapt to its ever-changing
environment.
Its multiple causes are all progressive, irreversible and harmful
ultimately leading to death
4. Cellular Ageing
Cellular Ageing is the progressive decline in cellular function
and viability caused by genetic abnormalities and the
accumulation of cellular and molecular damage due to the
effects of exposure to exogenous influences
6. Theories of Ageing
The knowledge regarding human ageing process is still obscure in some of its aspects
Many theories have been proposed to explain the process, but they are all specific of a
particular cause of ageing; a global view of them is needed
8. Evolutionary theory
• Accumulation of DNA mutations after several cell
cycles leads to cessation of further division
Mutation Accumulation
• Result of natural degrading process that leads to
accumulation of damage which can be repaired at the
expense of reproduction
Disposable soma
• Some traits that increase fitness early in life may also
have negative effects later in life.
Antagonistic pleiotropy
9. Molecular Theory
GENE REGULATION: Ageing is caused by changes in expression of genes regulation
CODON RESTRICTION: Accuracy of mRNA translation is impaired due to inability to
decode codon in mRNA.
ERROR CATASTROPHE: Decline in correct gene expression results in increased
fraction of abnormal proteins..
SOMATIC MUTATION: Molecular damage accumulates due to DNA damage.
DYSDIFFERENTIATION: Gradual accumulation of molecular damage impairs gene
expression. regulation.
10. Cellular Theory
TELOMERE THEORY : Senescence results from telomere loss with each cell cycle.
FREE RADICAL THEORY : Oxidative mechanisms produce highly reactive free
radicals that subsequently damage proteins, lipids, & DNA.
WEAR & TEAR THEORY : Accumulation of normal injury leads to senescence.
APOPTOSIS : Programmed cell death from genetic events or genome crisis
11. Systemic Theory
• Alterations in neuroendocrine control of
homeostasis results in ageingNEUROENDOCRINE
• Assumes a fixed amount of metabolic period
for every living organism. (LIVE FAST, DIE
YOUNG)
RATE OF LIVING
12. Theories of Ageing
The search for a single cause of ageing has recently been replaced by the view of ageing
as an extremely complex, multifactorial process.
Therefore, the different theories of aging are not mutually exclusive, but complementary
of others in the explanation of the normal aging process
18. DNA Repair and Senescence
Monitors integrity of
DNA before replication.
Pauses cell cycle
for DNA repair
G1/S
Monitors integrity of
DNA after replication so
that it can enter mitosis
DNA damaged beyond repair
Non-replicative state
(SENESCENCE)
G2/M
19. Telomeres
Cellular Senescence: Normal cells have a limited capacity for replication. After a fixed no. of
divisions cells become arrested in a terminally non dividing state, known as replicative
senescence
Chromosomes end with repeats of conserved ‘TTAGGG’ sequence - interact with specific
proteins -looped conformation- protects chromosomal DNA from degradation
23. Defective Protein homeostasis
Maintenance of protein quality, or proteostasis, is critical for the health and
longevity of the cell
Proteostasis ensures a supply of high-quality protein by culling misfolded and
damaged proteins from the cellular pool and replacing them with newly formed
proteins
Disruption of proteostasis is hastened by stress and signals organismal ageing
24. Chaperones, include small heat
shock proteins, as well as SOD
and catalase
direct AA chains to the correctly
folded state, misfolded proteins
to degradation pathways &
refold misfolded proteins
UPR monitors quality of
unfolded AA chains primarily in
the ER: ER-associated
degradation (ERAD) pathway
.
Molecular chaperones
25. Autophagy-Lysosome
System
► Autophagy is required for
longevity
► Inhibition of autophagy
generates hallmarks of aging at
an accelerated rate
► Autophagic clearing of
damaged proteins, protein
aggregates, organelles, lipids,
etc is required to provide new
raw material for a healthy cell.
26. Nutrient Sensing
Dietary restriction (DR), a reduction in food intake without malnutrition, extends the
average and/or maximum life span of various organisms
Causes a reduction in metabolic markers of several diseases, including diabetes,
cardiovascular disease and cancer increasing longevity
27. Insulin and insulin-like growth factor(IIS)
Caloric restriction
- “insulin and insulin-like growth factor”(IIS)
leads to increased life span and resistance to age-related pathologies
- Ribosomal S6 protein kinase 1 (S6K1)
RAS
FOXO, a transcription factor
- mammalian Target of Rapamycin
serine/threonine-protein kinase
AKT
28. Sirtuins
Sirtuins are a family of proteins that act as NAD(+) dependent histone deacetylases, which help
control gene expression coding for various proteins
Sirtuins detect when energy levels are low by sensing the coinciding increase of NAD+.
They also
help control catabolic metabolism
stimulate protein folding
inhibit harmful effects of ROS.
Upregulating sirtuins produces anti-aging or health-promoting effects
30. Disorders of Premature Ageing
HUTCHINSON GUILFORD PROGERIA
Male pattern baldness
Cataracts
Life span :10 yrs.
Mutation in LMNA gene (codes for protein Laminin A)
Defective precursor (PROGERIN)
Interferes with organisation of nuclear heterochromatin
which regulates expression of various genes
31. Disorders of Premature Ageing
ATAXIA TELENGIECTASIA
Manifestation of ageing at increased rate.
Mutation in gene encoding for protein involved in repairing double
stranded breaks in DNA.
32. Premature Ageing Disorders
DOWN’S SYNDROME
Patients generally age more rapidly.
Their fibroblasts are capable of fewer cell divisions in culture than those
from age matched controls.
The loss of telomeres was shown to be more rapid in lymphocytes
isolated from the blood of trisomic patients in accord with their more
rapid aging.
33. A list of syndromes carrying defect in genome maintenance
34. A list of syndromes carrying defect in Genome Maintenance
38. SENESCENCE –POSITIVE ASPECT
Senescence functions as a tumour suppressing
mechanism limiting cell proliferative capacity in vivo
implying that replicative senescence did not evolve to
cause ageing but is rather a consequence of a biological
device that suppresses tumour formation.
Aging can be considered at diff level. It can be…Aging of organism as a whole is studied
Aging of different cells
Gave The Theory of Programmed Death. He was one of the first scientist to use evolutionary arguments to explain aging. Harman proposed the Free Radical Theory of Aging in 1956 and in 1972 extended the idea, developing the "mitochondrial theory of aging" The cellular senescence theory of aging was formulated in 1965 by hayflick& moorhead. cell senescence was described as the process occurring in normal human cells in culture and characterized by a limited number of cell div
.despite the recent dev in science, the know……Many theories have been proposed of which the major ones can be devided into
The major and most accepted theories can be divided into
Evolutionary theory indicates aging as the result from a decline in the force of natural selection. ….. It was refuted until recently and is now agin being considered and studied….disposable soma theory of aging” argues that the somatic organism is effectively maintained only for reproductive success; afterwards it is disposable.
Free radical.it is among the most accepted theories of aging. It states that
Are subjected to indiscriminate dam such as …. Any acquired error leads to permanent damage which has an…
diet, lifestyle, drugs (e.g. tobacco and alcohol) and radiation etc. cause free radical production within the body.
However, there is also natural production of free-radicals within the body. This is the result of the production of ATP, particularly from the mitochondria, oxygen is a potent free-radical producer.
Free radicals attack the structure of cell membranes, which then create metabolic waste products. Such toxic accumulations interfere with cell communication, disturb DNA, RNA and protein synthesis,
Free radicals can however be transformed by free-radical scavengers
various agents cause different types of dna damage
cellular function relies heavily on the integrity of the genome, which must be preserved. This is why there are several DNA damage repair and checkpoint systems that enables cell survival or triggers senescence or cell death when DNA is damaged
Our chromosomes end with repeats of conserved ‘TTAGGG’ sequence known as telomeres. These sequences interact with specific proteins & attain a looped conformation- protects chromosomal DNA from degradation and fusion
When somatic cells replicate, a small section of the telomere is not duplicated and telomeres become progressively shortened. As the telomeres become shortend, the ends of ch. Are not protected and r seen as broken dna. Signalling cell cycle arrest
Telomere length can be prevented from shortening by an enzyme Telomerase. Telomerase is a specialized RNA-protein complex that uses its own RNA as a template for adding nucleotides to the ends of chromosomes
(a)Telomerase enzyme -active in germline and stem cells -and maintains their telomere length by adding ‘TTAGGG’ repeats to the ends of chromosomes. Therefore, telomeres do not shorten in these types of cells. (b) Telomerase- inactive in normal somatic cells- lose telomeres over time - length reaches below a critical limit- senesce or die(c) In the abs of appropriate signals, continued cell division leads to severe telomere shortening and genomic instability. Cells which survive this crisis, activate a telomere maintenance mechanism& become oncogenic & have very short but stable telomeres
Unfolded protein response
The second mechanism of protein homeostasis is the
It has been seen that DR Including caloric restriction (CR), restriction of major dietary components or intermittent fasting. Other than the indirect pathways, it also causes…
Major features of cellular aging. As the cell ages, translational defects & entropy progressively inc the amt of cell damage& clearance and quality ctrl mech grow less effective.
(a) In a young cell, most organelles are healthy& when proteins acquire damage, they are cleared either by ERAssoDegradation (in the ER) or autophagy (in the cytosol). (b) In an older cell, accumulated damage leads to a less healthy cell. ROS build up from damaged mitochondria and contribute to a greater fraction of the proteome consisting of damaged proteins and protein aggregates
Causing both accelerated ageing and cancer predisposition
Table 5shows a list of age related diseases with the indication of their approximate age of onset. Articular pathology, osteoarthritis starts the earliest. This original matrix is progressively destroyed and replaced by a fibrous matrix. Ensuing inflammation will continue to destroy the original cartilage matrix