Effects of Ferroptosis on Cardiovascular Diseases

Abstract

Ferroptosis is a novel form of programmed cell death characterized by the accumulation of iron-dependent lipid peroxides, which causes membrane injury. Under the catalysis of iron ions, cells deficient in glutathione peroxidase (GPX4) cannot preserve the balance in lipid oxidative metabolism, and the buildup of reactive oxygen species on the membrane lipids leads to cell death. An increasing body of evidence suggests that ferroptosis plays a significant role in the development and occurrence of cardiovascular diseases. In this paper, we mainly elaborated on the molecular mechanisms regulating ferroptosis and its impact on cardiovascular disease to lay the groundwork for future studies on the prophylaxis and treatment of this patient population.

Translational Potential of Baicalein in Mitigating RSL3-Induced Ferroptosis in Fibroblasts: Implications for Therapeutic Interventions

“…Moreover, ferroptosis is characterized by distinct morphological changes, including decreased mitochondrial volume, increased mitochondrial membrane density, and the absence of typical apoptotic features [4]. Dysregulation of ferroptosis has been linked to several illnesses including neurological conditions [5][6][7], cardiovascular diseases [8,9], acute and chronic kidney injury [10][11][12], ischemia-reperfusion injury [13,14], and cancer therapy [15][16][17], making it an active research topic in cell biology and medicine.…”