Wu Shengnan, Ding Ding, Wang Deguo
Department of Geriatrics, The First Affiliated Hospital of Wannan Medical College, 241001 Wuhu, Anhui, China.
Rev Cardiovasc Med. 2024 Oct 11;25(10):366. doi: 10.31083/j.rcm2510366. eCollection 2024 Oct.
Cardiac hypertrophy is characterized by an increased volume of individual cardiomyocytes rather than an increase in their number. Myocardial hypertrophy due to pathological stimuli encountered by the heart, which reduces pressure on the ventricular walls to maintain cardiac function, is known as pathological hypertrophy. This eventually progresses to heart failure. Certain varieties of regulated cell death (RCD) pathways, including apoptosis, pyroptosis, ferroptosis, necroptosis, and autophagy, are crucial in the development of pathological cardiac hypertrophy. This review summarizes the molecular mechanisms and signaling pathways underlying these RCD pathways, focusing on their mechanism of action findings for pathological cardiac hypertrophy. It intends to provide new ideas for developing therapeutic approaches targeted at the cellular level to prevent or reverse pathological cardiac hypertrophy.
心脏肥大的特征是单个心肌细胞体积增大,而非细胞数量增加。心脏因遇到病理刺激而发生的心肌肥大,可减轻心室壁压力以维持心脏功能,这种肥大被称为病理性肥大。这最终会发展为心力衰竭。某些类型的程序性细胞死亡(RCD)途径,包括凋亡、焦亡、铁死亡、坏死性凋亡和自噬,在病理性心脏肥大的发展过程中至关重要。本综述总结了这些RCD途径的分子机制和信号通路,重点关注它们在病理性心脏肥大中的作用机制研究结果。旨在为开发针对细胞水平的治疗方法以预防或逆转病理性心脏肥大提供新思路。