<p>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.</p> Graphical Abstract <p>Autophagy and ferroptosis-induced cell death are important causes of myocardial ischemia-reperfusion injury(MI/RI), and targeted modulation of cell death may be key to attenuating I/R injury. Increasing evidence suggests that autophagy, especially selective autophagy, plays an important role in promoting ferroptosis. There may be interactions between various selective autophagy that constitute a complex regulatory network between autophagy and ferroptosis, such as ferritinophagy, mitophagy, lipophagy, clockophagy, and chaperone-mediated autophagy (CMA). In addition, there are co-regulatory molecules of autophagy and ferroptosis during MI/RI, including Becline 1, NRF2, AMPK, mTOR, P53, PKA, AKT, STAT3, ERK1/2, and HIF. To date, the relationship between ferroptosis and autophagy in MI/RI is still in the preliminary research stage, and further studies will reveal the relationship between the two. Further studies in the future to clarify the interaction between autophagy and ferroptosis may provide a new direction for the treatment of MI/RI, which is of great clinical significance.</p> <p></p>