Ferroptosis: A novel paradigm in the pathophysiology of MINOCA
Myocardial infarction with non-obstructive coronary arteries (MINOCA) is a clinically distinct entity characterized by myocardial infarction without significant epicardial coronary artery stenosis. This heterogeneous syndrome, accounting for 5–15% of myocardial infarction cases, remains diagnostically and therapeutically challenging (1-3). While mechanisms such as microvascular dysfunction, coronary vasospasm, and plaque erosion have been proposed, recent evidence highlights ferroptosis—a regulated, iron-dependent form of cell death driven by lipid peroxidation—as a potential key contributor to cardiomyocyte injury and MINOCA pathophysiology.
