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SIRT4 prevents hypoxia-induced apoptosis in H9c2 cardiomyoblast cells.

Authors: Liu, B  Che, W  Xue, J  Zheng, C  Tang, K  Zhang, J  Wen, J  Xu, Y 
Citation: Liu B, etal., Cell Physiol Biochem. 2013;32(3):655-62. doi: 10.1159/000354469. Epub 2013 Sep 10.
Pubmed: (View Article at PubMed) PMID:24029877
DOI: Full-text: DOI:10.1159/000354469

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.


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CRRD Object Information
CRRD ID: 9586053
Created: 2014-09-26
Species: All species
Last Modified: 2014-09-26
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.