Irisin improves ROS‑induced mitohormesis imbalance in H9c2 cells

Area of Science:

• Cardiology
• Cell Biology
• Mitochondrial Biology

Background:

• Abnormal mitohormesis contributes to cardiac diseases like hypertrophy and heart failure.
• Irisin, a myokine, offers cardioprotection against oxidative stress injury.

Purpose of the Study:

• To investigate irisin's role in mitigating oxidative stress-induced cardiac cell damage.
• To explore the involvement of the PGC-1α pathway in irisin's cardioprotective effects.

Main Methods:

• Established an oxidative stress model in H9c2 rat cardiomyocyte cells using hydrogen peroxide (H2O2).
• Assessed mitochondrial membrane potential, reactive oxygen species (ROS), and mitohormesis factors.
• Utilized siRNA interference for peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) to study its role.

Main Results:

• Irisin partially improved mitochondrial membrane potential and ROS levels under oxidative stress.
• Irisin upregulated mitochondrial fusion proteins (OPA1, Mfn2) and downregulated fission protein (DRP1).
• Irisin promoted mitochondrial biosynthesis via PGC-1α, increasing OPA1 mRNA and COX4 protein levels.

Conclusions:

• Irisin partially mitigates oxidative stress-induced cardiac cell damage independently of the PGC-1α pathway.
• Irisin maintains cardiac energy metabolism by improving mitochondrial structure and function.
• Irisin demonstrates potential as a therapeutic agent for cardiac diseases linked to oxidative stress.