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Updated: May 7, 2026
In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
Published on: October 27, 2020
SIRT4 prevents hypoxia-induced apoptosis in H9c2 cardiomyoblast cells
Ban Liu1, Wenliang Che, Jinsong Xue
1Department of Cardiology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, P.R. China.
Aims:
Apoptosis plays a critical role in cardiomyocyte loss during ischaemic heart injury. A detailed understanding of the mechanism involved has a substantial impact on the optimization and development of treatment strategies. Here, we report that the expression of SIRT4, a mitochondrial sirtuin, is markedly down-regulated in hypoxia-induced apoptosis of H9c2 cardiomyoblast cells.
Methods And Results:
SIRT4 interference significantly alters H9c2 cell viability, apoptotic cell number and caspase-3/7 activity. Furthermore, SIRT4 expression can affect the ratio of pro-caspase 9/caspase 9 or pro-caspase 3/caspase 3, an affect Bax translocation, which in turn alters the development of H9c2 cell apoptosis.
Conclusion:
These results suggest that SIRT4 is a key player in hypoxia-induced cardiomyocyte apoptosis, and that strategies based on its enhancement might be of benefit in the treatment of ischaemic heart disease.
Insights
Mitochondrial SIRT4 is downregulated in heart cells during hypoxia. Enhancing SIRT4 may offer new treatments for heart injury by reducing apoptosis.
Area of Science:
- Cardiovascular Biology
- Mitochondrial Function
- Cell Death Pathways
Background:
- Apoptosis is crucial in cardiomyocyte loss during ischemic heart injury.
- Understanding these mechanisms is vital for developing effective treatments.
- SIRT4, a mitochondrial sirtuin, is implicated in cellular stress responses.
Purpose of the Study:
- To investigate the role of SIRT4 in hypoxia-induced apoptosis of H9c2 cardiomyoblast cells.
- To determine if SIRT4 expression is altered under hypoxic conditions.
- To explore the impact of SIRT4 modulation on apoptotic pathways.
Main Methods:
- Utilized H9c2 cardiomyoblast cells exposed to hypoxic conditions.
- Assessed SIRT4 expression levels.
- Performed functional assays to evaluate cell viability, apoptosis, and caspase activity.
- Investigated the effects on caspase and Bax translocation.
Main Results:
- SIRT4 expression was significantly downregulated in H9c2 cells under hypoxia.
- SIRT4 interference altered cell viability and increased apoptotic cell numbers.
- Modulation of SIRT4 affected caspase-3/7 activity and the pro-caspase/caspase ratios.
- SIRT4 influenced Bax translocation, a key event in apoptosis.
Conclusions:
- SIRT4 is a critical regulator in hypoxia-induced cardiomyocyte apoptosis.
- Downregulation of SIRT4 exacerbates apoptotic cell death.
- Strategies aimed at enhancing SIRT4 may provide a therapeutic approach for ischemic heart disease.