Ferritinophagy and ferroptosis in cardiovascular disease: Mechanisms and potential applications.

Ferroptosis is a type of regulated cell death driven by iron dependent accumulation of cellular reactive oxygen species (ROS) when glutathione (GSH)-dependent lipid peroxidation repair systems are compromised. Nuclear receptor co-activator 4 (NCOA4)-mediated selective autophagy of ferritin, termed ferritinophagy, involves the regulation of ferroptosis. Emerging evidence has revealed that ferritinophagy and ferroptosis exert a significant role in the occurrence and development of cardiovascular disease. In the present review, we aimed to present a brief overview of ferritinophagy and ferroptosis focusing on the underlying mechanism and regulations involved. We summarize and discuss relevant research progress on the role of ferritinophagy and ferroptosis in cardiovascular diseases accompanied with potential applications of ferritinophagy and ferroptosis modulators in the treatment of ferroptosis-associated cardiovascular diseases. [Display omitted] • Ferroptosis is a novel form of iron-dependent nonapoptotic regulated cell death. • Iron dependent lipid peroxidation by xCT/GPX4 is the hallmark of ferroptosis. • Ferritinophagy induces ferroptosis and involves in cardiovascular disorders. • Pharmacological modulators of ferroptosis exert cardiovascular therapeutic effect. [ABSTRACT FROM AUTHOR]