Kisspeptin-10 alleviates OGD/R-induced H9c2 cardiomyocyte injury by triggering autophagy via regulating the YY1/TFEB axis.

Authors

Qintong Li, Huayu Liu, Yinying He, Yong Xie, Jingting Mai, Tucheng Huang, Fuwen Huang

Published in

Cytotechnology. Volume 78. Issue 6. Pages 212. Epub Oct 12, 2026.

Abstract

Myocardial ischemia-reperfusion injury (MIRI) is characterized by exacerbated myocardial damage following the restoration of blood flow after myocardial ischemia, owing to factors such as increased production of reactive oxygen species, calcium overload, and inflammatory responses. Induction of cellular autophagy has been reported to alleviate MIRI. Kisspeptin-10 (Kp-10) is a short peptide produced by hydrolysis of the precursor protein encoded by the KISS1 gene and has shown promising autophagy-inducing properties. Here, the effects of Kp-10 on OGD/R-induced injury were investigated in H9c2 cardiomyocytes using an in vitro model relevant to MIRI. H9c2 cardiomyocytes were treated with OGD/R, followed by incubation with 50 or 100 nM Kp-10. Markedly reduced cell viability, an increased apoptotic rate and MDA levels, and diminished SOD and CAT activities were observed in OGD/R-stimulated H9c2 cardiomyocytes. These changes were accompanied by downregulated LC3-II/I, ATG5, and Beclin1, decreased nuclear levels of YY1 and TFEB, and reduced transcriptional activities of YY1 and TFEB, all of which were remarkably reversed by Kp-10. Moreover, the effects of Kp-10 on cell viability, oxidative stress, and the expression of autophagy-related proteins were substantially abolished by silencing YY1 or TFEB. Collectively, Kp-10 attenuated OGD/R-induced H9c2 cardiomyocyte injury in vitro, possibly by enhancing autophagy through the YY1/TFEB axis. These findings provide a cellular basis for further investigation of Kp-10 in MIRI, although validation in animal models is required before its clinical relevance can be assessed.
The online version contains supplementary material available at https://doi.org/10.1007/s10616-026-01089-2.

PMID:
42871171
Bibliographic data and abstract were imported from PubMed on 14 Oct 2026.

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