Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

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.

Annotation

Gene Ontology Annotations
Objects Annotated

Additional Information

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



NHLBI Logo

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