03Oct 2024
Ferroptosis and Mitophagy in Myocardial Ischemia-Reperfusion Injury

Ferroptosis and Mitophagy in Myocardial Ischemia-Reperfusion Injury

Myocardial ischemia-reperfusion injury (MI/RI) significantly contributes to myocardial damage post-acute myocardial infarction, with ferroptosis playing a crucial role. The study investigated how MI/RI induces myocardial injury by inhibiting the ferroptosis-related SLC7A11/GSH/GPX4 pathway and activating mitophagy. Using a rat MI/RI model and cultured H9C2 cardiomyocytes, we demonstrated that downregulation of SLC7A11 impairs GSH synthesis and GPX4 activity, promoting ferroptosis. Additionally, hypoxia/reoxygenation (H/R) activated mitophagy, further exacerbating ferroptosis. Treatment with lipoxstatin-1 and overexpression of SLC7A11 reduced cell death by preserving the GSH/GPX4 pathway. Mitophagy inhibition also reversed H/R-induced ferroptosis. These findings suggest that ROS-mediated activation of mitophagy suppresses the SLC7A11/GSH/GPX4 pathway, contributing to cardiomyocyte injury.

  • #cardiology

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