Acute Hypoxia Induces Cardiomyocyte Autophagy via SIRT5/mTOR/ULK1 Pathway.

Authors

Yunle Wang, Hongqi Wei, Yuxuan Wu, Yang Luo

Published in

BioMed research international. Volume 2026. Issue 1. Pages e8867024.

Abstract

The aim of this study is to investigate the expression of SIRT5 in acute myocardial hypoxia and to further explore its function during this pathological process.
We analyzed the microarray dataset GSE27975 derived from the Gene Expression Omnibus (GEO) database and identified differentially expressed genes (DEGs) between hypoxic and normoxic cardiomyocytes. We divided C57BL/6 J mice into two groups: the sham group and the acute myocardial infarction (MI) group. Heart functions were detected by echocardiogram, and heart tissue was harvested on the 3rd day after MI for the detection of autophagy and SIRT5 expression. To further study the mechanism of Sirt5 in hypoxic cardiomyocytes, we divided H9C2 cells into four groups: the control group, the hypoxia group, the Sirt5-knockdown group and the Sirt5-knockdown + hypoxia group and detected Sirt5 expression, cell autophagy and potential pathway.
A total of 156 genes were highly expressed, and 185 genes were expressed at low levels between hypoxic and normoxic cardiomyocytes. SIRT5 was expressed at low levels in the hypoxia group. In vivo, we generated the MI mouse model, and heart function was decreased. The expression of SIRT5 in heart tissue was decreased after MI, whereas the autophagy level was increased. In vitro, after we knocked down Sirt5 in H9C2 cardiomyocytes, autophagy was significantly increased. Meanwhile the expression of p-mTOR and p-ULK1 changed, whereas both mitochondrial membrane potential and respiratory capacity were maintained.
Acute hypoxia reduces SIRT5 expression may be associated with cardiomyocyte autophagy. Knockdown Sirt5 in H9C2s could activate autophagy via mTOR/ULK1 pathway and preserve mitochondrial function.

PMID:
42852985
Bibliographic data and abstract were imported from PubMed on 09 Oct 2026.

Read full publication at:
Please sign in to see all details.

Stats

1-terrible, 9-excellent. How would you rate this publication? Sign in in to submit your rating.

Post a comment

You need to be signed in to post comments. You can sign in here.

Comments

There are no comments yet.