Institute for Translational Medicine, Qingdao University, Deng Zhou Road 38, Qingdao, 266021, China.
Cell Mol Life Sci. 2018 Jan;75(2):291-300. doi: 10.1007/s00018-017-2640-8. Epub 2017 Sep 14.
Loss of functional cardiomyocytes is a major underlying mechanism for myocardial remodeling and heart diseases, due to the limited regenerative capacity of adult myocardium. Apoptosis, programmed necrosis, and autophagy contribute to loss of cardiac myocytes that control the balance of cardiac cell death and cell survival through multiple intricate signaling pathways. In recent years, non-coding RNAs (ncRNAs) have received much attention to uncover their roles in cell death of cardiovascular diseases, such as myocardial infarction, cardiac hypertrophy, and heart failure. In addition, based on the view that mitochondrial morphology is linked to three types of cell death, ncRNAs are able to regulate mitochondrial fission/fusion of cardiomyocytes by targeting genes involved in cell death pathways. This review focuses on recent progress regarding the complex relationship between apoptosis/necrosis/autophagy and ncRNAs in the context of myocardial cell death in response to stress. This review also provides insight into the treatment for heart diseases that will guide novel therapies in the future.
功能性心肌细胞的丧失是心肌重构和心脏病的主要潜在机制,这是由于成年心肌的再生能力有限。凋亡、程序性坏死和自噬导致心肌细胞丧失,通过多种复杂的信号通路控制心肌细胞死亡和细胞存活的平衡。近年来,非编码 RNA(ncRNA)受到了广泛关注,以揭示它们在心血管疾病细胞死亡中的作用,如心肌梗死、心肌肥厚和心力衰竭。此外,基于线粒体形态与三种细胞死亡类型相关的观点,ncRNA 能够通过靶向参与细胞死亡途径的基因来调节心肌细胞的线粒体分裂/融合。本综述重点介绍了应激状态下心肌细胞死亡中凋亡/坏死/自噬与 ncRNA 之间复杂关系的最新进展。本综述还为心脏病的治疗提供了新的见解,为未来的新疗法提供了指导。