Programmed death of cardiomyocytes in cardiovascular disease and new therapeutic approaches

Abstract

Cardiovascular diseases (CVDs) have a complex pathogenesis and pose a major threat to human health. Cardiomyocytes have a low regenerative capacity, and their death is a key factor in the morbidity and mortality of many CVDs. Cardiomyocyte death can be regulated by specific signaling pathways known as programmed cell death (PCD), including apoptosis, necroptosis, autophagy, pyroptosis, and ferroptosis, etc. Abnormalities in PCD can lead to the development of a variety of cardiovascular diseases, and there are also molecular-level interconnections between different PCD pathways under the same cardiovascular disease model. Currently, the link between programmed cell death in cardiomyocytes and cardiovascular disease is not fully understood. This review describes the molecular mechanisms of programmed death and the impact of cardiomyocyte death on cardiovascular disease development. Emphasis is placed on a summary of drugs and potential therapeutic approaches that can be used to treat cardiovascular disease by targeting and blocking programmed cell death in cardiomyocytes.

Keywords: Atorvastatin (PubChem CID: 60823); Cardiomyocyte; Cardiovascular diseases; Carvedilol (PubChem CID: 2585); Dapagliflozin (PubChem CID: 9887712); Dexmedetomidine (PubChem CID:6918081); Drug; Fluvastatin (PubChem CID: 23679527); Melatonin (PubChem CID:896); Probucol (PubChem CID: 4912); Programmed cell death; SP600125 (PubChem CID: 8515); Scutellarin (PubChem CID: 185617); Treatment; Trimetazidine (PubChem CID: 83201).