Evidence map›Paper›PMID 42852985›Full record

ArticleBioMed research international2026

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

Yunle Wang, Hongqi Wei, Yuxuan Wu, Yang Luo

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Article in BioMed research international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

4 authors.

Yunle WangGeriatrics Department, Shanghai Health and Medical Center, Wuxi, Jiangsu, China.ORCID https://orcid.org/0009-0001-6792-2312
Hongqi WeiOtorhinolaryngology Department, Suzhou Dushu Lake Hospital, Suzhou, Jiangsu, China.
Yuxuan WuMedical College, Suzhou University, Suzhou, Jiangsu, China, usts.edu.cn.
Yang LuoRadiology Department, Shanghai Health and Medical Center, Wuxi, Jiangsu, China.

Funding

NSFC Young Fund 81900312Shanghai Public Health Research Special Program 2026GKM18Shanghai "Rising Stars of Medical Talents" Youth Development Program SHWSRS (2023)_062
6 · The paper itself

Abstract

objectiveThe 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. MATERIAL AND

methodsWe 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.

resultsA 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.

conclusionAcute 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.

Indexed as

AutophagyAutophagy-Related Protein-1 HomologHypoxiaIntracellular Signaling Peptides and ProteinsMyocytes, CardiacSirtuinsTOR Serine-Threonine KinasesAnimalsCell HypoxiaCell LineMaleMiceMice, Inbred C57BLMyocardial InfarctionRatsSignal TransductionAutophagy-Related Protein-1 HomologIntracellular Signaling Peptides and ProteinsmTOR protein, mouseSirtuinsTOR Serine-Threonine KinasesUlk1 protein, mouseacute myocardial infarctionautophagyhypoxiamitochondrialmTORSIRT5

Identifiers

PMID42852985

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.