This document discusses apoptosis in cardiomyocytes and the roles of sulfur dioxide (SO2) and cyclophilin D (CypD) in regulating apoptosis. It aims to study the effects of SO2 and isoproterenol (ISO) treatment on apoptosis in cardiomyocytes. The results found that SO2 treatment alone significantly decreased apoptosis in cardiomyocytes and caspase 9 expression. ISO treatment increased apoptosis but to a lesser extent than when combined with SO2. The conclusions discuss how increasing endogenous SO2 production in cardiomyocytes could help prevent apoptosis and cardiac output decline with age, but this would require further molecular biology studies to understand the mechanisms and inhibit apoptosis without side effects.

1. Jose David Rodriguez Henao Third semester
Universidad Pontificia Polivariana

2. INTRODUCTION
APOPTOSIS
● Programed death cell
● Damaged cells
● Need to keep sane the body
https://concepto.de/apoptosis/

3. INTRODUCTION
CypD
cyclophilin d
● protein that binds
ciclosporins
● located in the
mitochondrial matrix
● acts as an important
regulator of switching
the mPTP opening

4. GENERAL OBJETIVE

5. METHODS
● Transcription
● Cell culture

6. METHODS the basis and why they do this
● Western blot
● Immunofluorescence

7. —SOMEONE FAMOUS
RESULTADOS

8. RESULTADOS

9. DISCUSSIONS
AUTHOR
Huang et al
WHAT AUTHOR SAYS
“Previously, SO2 was considered to
be a toxic gas and environmental
pollutant. In recent years, it is
shown that the SO2 can be
endogenously synthesized by an
enzymatic reaction catalyzed by
AAT in cardiovascular tissues”
ARE THE WRITER AGREE?
- Endogenous SO2 exerts important
cardiovascular effects. For example, the
reduction of endogenous SO2 promotes the
proliferation and migration of cardiac
fibroblasts (Zhang et al., 2018).
- Endogenous SO2 alleviates angiotensin
II-induced myocardial hypertrophy and
cardiomyocyte autophagy (Chen et al., 2016).
- It was reported that the downregulated
endogenous SO2/AAT pathway might be
involved in the possible mechanisms
underlying the myocardial injury. Liang et al
found that the in vivo protective effect of SO2
on the myocardial injury was related to the
increased myocardial antioxidant capacity
(Liang et al., 2011).

10. 2
1
CONCLUSIONS
SO2 and cardiomyocyte
If we can go up the
endogen production of SO2 in the
cardiomyocytes we could prevent
apoptosis and fall down the
cardiac output that Is produced by
the years, but we only do this with
the implement of molecular biology
to study and know the function of
the mechanism and how to inhibit
it without causing malformations
Caspase 9 and apoptosis
The inhibition of caspase 9 and
CYPD its fundamental to reduces
de apoptosis in cardiomyocytes
and the only way to inhibit the
caspase 9 is using models of
molecular biology

11. APOPTOSIS IN
CARDIOMYOCYTES
USING SO2 USING ISO
USING SO2 + ISO
A big decrease of
apoptosis in
cardiomyocytes
Apoptosis decrease but
not much compared
with only SO2
The apoptosis in cardiomyocytes increase plus
the expression of caspase 9
The apoptosis in
cardiomyocytes increase
plus the expression of
caspase 9