Necroptosis: a significant and promising target for intervention of cardiovascular disease.

Due to changes in dietary structures, population aging, and the exacerbation of metabolic risk factors, the incidence of cardiovascular disease continues to rise annually, posing a significant health burden worldwide. Cell death plays a crucial role in the onset and progression of cardiovascular diseases. As a regulated endpoint encountered by cells under adverse stress conditions, the execution of necroptosis is regulated by classicalpathways, the calmodulin-dependent protein kinases (CaMK) pathway, and mitochondria-dependent pathways, and implicated in various cardiovascular diseases, including atherosclerosis, myocardial infarction, myocardial ischemia-reperfusion injury (IRI), heart failure, diabetic cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, chemotherapy drug-induced cardiomyopathy, and abdominal aortic aneurysm (AAA). To further investigate potential therapeutic targets for cardiovascular diseases, we also analyzed the main molecules and their inhibitors involved in necroptosis in an effort to uncover insights for treatment.