Regulated cell death in acute myocardial infarction: Molecular mechanisms and therapeutic implications
- Ageing Res Rev. 2025 Feb:104:102629. doi: 10.1016/j.arr.2024.102629.
- 1. Department of Pathology, Hunan Cancer Hospital, the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China.
- 2. Department of Pathophysiology, School of Basic Medical Science, Central South University, Changsha, Hunan, China; Key Laboratory of Sepsis Translational Medicine of Hunan, Central South University, Changsha, Hunan, China; National Medicine Functional Experimental Teaching Center, Central South University, Changsha, Hunan, China.
- 3. Department of Pathophysiology, School of Basic Medical Science, Central South University, Changsha, Hunan, China; Key Laboratory of Sepsis Translational Medicine of Hunan, Central South University, Changsha, Hunan, China; National Medicine Functional Experimental Teaching Center, Central South University, Changsha, Hunan, China. Electronic address: [email protected].
Acute Myocardial Infarction (AMI), primarily caused by coronary Atherosclerosis, initiates a series of events that culminate in the obstruction of coronary arteries, resulting in severe myocardial ischemia and hypoxia. The subsequent myocardial ischemia/reperfusion (I/R) injury further aggravates cardiac damage, leading to a decline in heart function and the risk of life-threatening complications. The complex interplay of multiple regulated cell death (RCD) pathways plays a pivotal role in the pathogenesis of AMI. Each RCD pathway is orchestrated by a symphony of molecular regulatory mechanisms, highlighting the dynamic changes and critical roles of key effector molecules. Strategic disruption or inhibition of these molecular targets offers a tantalizing prospect for mitigating or even averting the onset of RCD, thereby limiting the extensive loss of cardiomyocytes and the progression of detrimental myocardial fibrosis. This review systematically summarizes the mechanisms underlying various forms of RCD, provides an in-depth exploration of the pathogenesis of AMI through the lens of RCD, and highlights a range of promising therapeutic targets that hold the potential to revolutionize the management of AMI.