The link between ferroptosis and autophagy in myocardial ischemia/reperfusion injury: new directions for therapy.

Abstract

Myocardial ischemia/reperfusion (I/R)-induced cell death, such as autophagy and ferroptosis, is a major contributor to cardiac injury. Regulating cell death may be key to mitigating myocardial ischemia/reperfusion injury (MI/RI). Autophagy is a crucial physiological process involving cellular self-digestion and compensation, responsible for degrading excess or malfunctioning long-lived proteins and organelles. During MI/RI, autophagy plays both "survival" and "death" roles. A growing body of research indicates that ferroptosis is a type of autophagy-dependent cell death. This article provides a comprehensive review of the functions of autophagy and ferroptosis in MI/RI, as well as the molecules mediating their interaction. Understanding the link between autophagy and ferroptosis may offer new therapeutic directions for MI/RI, bearing significant clinical implications.