Irisin improves ROS‑induced mitohormesis imbalance in H9c2 cells.

Abnormal mitohormesis is a key pathogenic mechanism that induces a variety of cardiac diseases, including cardiac hypertrophy and heart failure. Irisin as a muscle factor serves a cardioprotective role in response to cellular oxidative stress injury. Rat cardiomyocyte cells (H9c2) were treated with 40 µM exogenous H(2)O(2) to establish an oxidative stress model, followed by addition of 75 nM exogenous irisin for experiments to determine mitochondrial membrane potential, reactive oxygen species, and Mitohormesis‑related factors by attrition cytometry. Subsequently, the expression of mitochondrial membrane potential, reactive oxygen species and Mitohormesis‑related factors were continued to be determined by establishing a peroxisome proliferator‑activated receptor γ coactivator‑1 alpha (PGC‑1α) siRNA interference model and continuing the treatment with the addition of 75 nM irisin 12 h before the end of interference. When H9c2 cells underwent oxidative stress, irisin partially improved mitochondrial membrane potential and reactive oxygen species levels and partially restored mitochondrial energy metabolism by upregulating fusion proteins optic atrophy 1 (OPA1) mitochondrial dynamin‑like GTPase and mitofusin 2 and downregulating fission protein dynamin‑related protein 1. Following interference with PGC‑1α, irisin promoted mitochondrial biosynthesis by increasing the mRNA levels of OPA1 and protein levels of cytochrome c oxidase subunit 4. These results suggested that irisin acted partially independently of the PGC‑1α signaling pathway to regulate mitohormesis imbalance due to oxidative stress and maintain energy metabolism by improving mitochondrial structure.