FGF21 Blunts Cardiac Ischemia/Reperfusion Injury by Promoting Autophagic Flux Via Stat1/Irgm1 Pathway.

Authors

Tao Tu, Zuodong Ning, Yuhu He, Yingxu Ma, Yichao Xiao, Zhaowei Zhu, Liang Tang, Xuping Li, Hui Yang, Mingxian Chen, Shi Tai, Qiming Liu, Shenghua Zhou

Published in

Journal of cardiovascular translational research. Oct 02, 2025. Epub Oct 02, 2025.

Abstract

This study aimed to investigate the underlying mechanisms of Fibroblast Growth Factor 21 (FGF21) in myocardial ischemia/reperfusion (I/R) injury. First, FGF21 was upregulated in the serum of patients with myocardial I/R injury as well as in I/R hearts of mice and hypoxia/reoxygenation (H/R) neonatal rat cardiomyocytes (NRCMs). While FGF21 knockout exacerbated such injury, which was mitigated by rhFGF21. Bioinformatics analysis identified immunity-related GTPase M1 (Irgm1) as a key autophagy-related gene downregulated in ventricular tissue of FGF21^-/- I/R mice. Impaired autophagic flux in FGF21^-/- mice during I/R could be rescued by rhFGF21 through the signal transducers and activators of transcription 1 (STAT1) pathway. The beneficial effects of rhFGF21 in reducing H/R injury were limited in Irgm1 knockdown NRCMs. This study suggested that FGF21 deficiency intensifies myocardial I/R injury by exacerbating the impairment of autophagic flux. Activation of FGF21 or Irgm1 may serve as a promising therapeutic strategy for myocardial I/R injury.

PMID:
41037149
Bibliographic data and abstract were imported from PubMed on 02 Oct 2025.

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