Exogenous hydrogen sulfide inhibits the senescence of cardiomyocytes through modulating mitophagy in rats

Jinghui Hao; Yuxin Xi; Lijie Jiao; Xin Wen; Ren Wu; Guiquan Chang; Fengqi Sun; Can Wei; Hongzhu Li

doi:10.1016/j.cellsig.2022.110465

Exogenous hydrogen sulfide inhibits the senescence of cardiomyocytes through modulating mitophagy in rats

Cell Signal. 2022 Dec:100:110465. doi: 10.1016/j.cellsig.2022.110465. Epub 2022 Sep 7.

Authors

Jinghui Hao¹, Yuxin Xi¹, Lijie Jiao², Xin Wen³, Ren Wu⁴, Guiquan Chang¹, Fengqi Sun¹, Can Wei¹, Hongzhu Li⁵

Affiliations

¹ Department of Pathophysiology, Harbin Medical University, Harbin 150081, Heilongjiang, China.
² School of Medicine, Xiamen University, Xiamen 361102, Fujian, China.
³ Department of Pathophysiology, Harbin Medical University, Harbin 150081, Heilongjiang, China; Department of Pathology, Jinan Central Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250013, Shandong, China.
⁴ Department of Pathophysiology, Harbin Medical University, Harbin 150081, Heilongjiang, China; School of Medicine, Xiamen University, Xiamen 361102, Fujian, China.
⁵ Department of Pathophysiology, Harbin Medical University, Harbin 150081, Heilongjiang, China; School of Medicine, Xiamen University, Xiamen 361102, Fujian, China. Electronic address: lhz2020@xmu.edu.cn.

PMID: 36087824
DOI: 10.1016/j.cellsig.2022.110465

Abstract

Hydrogen sulfide (H₂S), a gaseous molecule, has been shown to be involved in the regulation of body pathophysiological processes. Aging is related to structural and functional alterations within the heart. There is evidence that diminished mitophagy accelerates the aging process. Studies in recent years have revealed that plasma levels of H₂S in humans and old rats decrease with age, and H₂S acts as a cytoprotective mediator in the aging process. However, it is unclear whether H₂S can delay the senescence of cardiomyocytes by regulating mitophagy. Our present results showed that exogenous H₂S inhibited mitochondrial damage, oxidative stress and cell apoptosis, and enhanced mitophagy through upregulating the SIRT1-PINK1-parkin pathway in myocardial tissues of aged rats and cultured aged cardiomyocytes. Furthermore, the effect of exogenous H₂S on the above indicators was the same as that of SRT1720 (a SIRT1 agonist) and kinetin (a PINK1 activator). Our findings suggest that exogenous H₂S inhibits the senescence of cardiomyocytes by increasing mitophagy via upregulation of the SIRT1-PINK1-parkin pathway in rats.

Keywords: Cardiomyocytes; Hydrogen sulfide; Mitophagy; Rats; Senescence.