Acetylation, ferroptosis, and their potential relationships: Implications in myocardial ischemia-reperfusion injury

Abstract

Myocardial ischemia-reperfusion injury (MIRI) is a serious complication affecting the prognosis of patients with myocardial infarction and can cause cardiac arrest, reperfusion arrhythmias, no-reflow, and irreversible myocardial cell death. Ferroptosis, an iron-dependent, peroxide-driven, non-apoptotic form of regulated cell death, plays a vital role in reperfusion injury. Acetylation, an important post-translational modification, participates in many cellular signaling pathways and diseases, and plays a pivotal role in ferroptosis. Elucidating the role of acetylation in ferroptosis may therefore provide new insights for the treatment of MIRI. Here, we summarized the recently discovered knowledge about acetylation and ferroptosis in MIRI. Finally, we focused on the acetylation modification during ferroptosis and its potential relationship with MIRI.

Keywords: Acetylation; Ferroptosis; Histone deacetylases; Myocardial ischemia-reperfusion injury; Regulated cell death.