Ferroptosis and its emerging roles in cardiovascular diseases.

Ferroptosis is a new form of regulated cell death (RCD) driven by iron-dependent lipid peroxidation, which is morphologically and mechanistically distinct from other forms of RCD including apoptosis, autophagic cell death, pyroptosis and necroptosis. Recently, ferroptosis has been found to participate in the development of various cardiovascular diseases (CVDs) including doxorubicin-induced cardiotoxicity, ischemia/reperfusion-induced cardiomyopathy, heart failure, aortic dissection and stroke. Cardiovascular homeostasis is indulged in delicate equilibrium of assorted cell types composing the heart or vessels, and how ferroptosis contributes to the pathophysiological responses in CVD progression is unclear. Herein, we reviewed recent discoveries on the basis of ferroptosis and its involvement in CVD pathogenesis, together with related therapeutic potentials, aiming to provide insights on fundamental mechanisms of ferroptosis and implications in CVDs and associated disorders.

Li N ，Jiang W ，Wang W ，Xiong R ，Wu X ，Geng Q ... -  《-》

Emerging regulatory mechanisms in cardiovascular disease: Ferroptosis.

Ferroptosis, distinct from apoptosis, necrosis, autophagy, and other types of cell death, is a novel iron-dependent regulated cell death characterized by the accumulation of lipid peroxides and redox imbalance with distinct morphological, biochemical, and genetic features. Dysregulation of iron homeostasis, the disruption of antioxidative stress pathways and lipid peroxidation are crucial in ferroptosis. Ferroptosis is involved in the pathogenesis of several cardiovascular diseases, including atherosclerosis, cardiomyopathy, myocardial infarction, ischemia-reperfusion injury, abdominal aortic aneurysm, aortic dissection, and heart failure. Therefore, a comprehensive understanding of the mechanisms that regulate ferroptosis in cardiovascular diseases will enhance the prevention and treatment of these diseases. This review discusses the latest findings on the molecular mechanisms of ferroptosis and its regulation in cardiovascular diseases, the application of ferroptosis modulators in cardiovascular diseases, and the role of traditional Chinese medicines in ferroptosis regulation to provide a comprehensive understanding of the pathogenesis of cardiovascular diseases and identify new prevention and treatment options.

Jin S ，Wang H ，Zhang X ，Song M ，Liu B ，Sun W ... -  《-》

The Emerging Role of Noncoding RNA Regulation of the Ferroptosis in Cardiovascular Diseases.

Cardiovascular disease (CVD) is a significant public health issue due to its high prevalence and considerable contribution to the global disease burden. Recent studies suggest that genetic factors, including noncoding RNAs, have an important role in the progression of CVD. Noncoding RNA plays a critical role in genetic programming and gene regulation during development. Ferroptosis is a form of iron-dependent regulated cell death (RCD), which is mainly caused by increased lipid hydroperoxide and redox imbalance. Ferroptosis is essentially different from other forms of RCD in morphology and mechanism, such as apoptosis, autophagic cell death, pyroptosis, and necroptosis. Much evidence suggested ferroptosis is involved in the development of various CVDs, especially in cardiac ischemia/reperfusion injury, heart failure, and aortic dissection. Here, we review the latest findings based on noncoding RNA regulation of ferroptosis and its involvement in the pathogenesis of CVD and related treatments, aimed at providing insights into the impact of noncoding RNA regulation of ferroptosis for CVD.

Zhang J ，Liu X ，Li X ，Cai Y ，Zhou Y ，Wang Q ，Xu Z ，Xia P ，Yang P ，Jun L ，Yu P ，Shi A ... -  《-》

Noncoding RNAs regulating ferroptosis in cardiovascular diseases: novel roles and therapeutic strategies.

Wu C ，Bao S ，Sun H ，Chen X ，Yang L ，Li R ，Peng Y ... -  《-》

Decoding ferroptosis: Revealing the hidden assassin behind cardiovascular diseases.

The discovery of regulatory cell death processes has driven innovation in cardiovascular disease (CVD) therapeutic strategies. Over the past decade, ferroptosis, an iron-dependent form of regulated cell death driven by excessive lipid peroxidation, has been shown to drive the development of multiple CVDs. This review provides insights into the evolution of the concept of ferroptosis, the similarities and differences with traditional modes of programmed cell death (e.g., apoptosis, autophagy, and necrosis), as well as the core regulatory mechanisms of ferroptosis (including cystine/glutamate transporter blockade, imbalance of iron metabolism, and lipid peroxidation). In addition, it provides not only a detailed review of the role of ferroptosis and its therapeutic potential in widely studied CVDs such as coronary atherosclerotic heart disease, myocardial infarction, myocardial ischemia/reperfusion injury, heart failure, cardiomyopathy, and aortic aneurysm but also an overview of the phenomenon and therapeutic perspectives of ferroptosis in lesser-addressed CVDs such as cardiac valvulopathy, pulmonary hypertension, and sickle cell disease. This article aims to integrate this knowledge to provide a comprehensive view of ferroptosis in a wide range of CVDs and to drive innovation and progress in therapeutic strategies in this field.

Zhang Z ，Yang Z ，Wang S ，Wang X ，Mao J ... -  《-》