Health Management Center, The Third Xiangya Hospital of Central South University, Changsha, 410013, China.
Department of Cardiology, The Third Xiangya Hospital of Central South University, Changsha, 410013, China.
Mol Med. 2024 Sep 3;30(1):137. doi: 10.1186/s10020-024-00901-z.
N6-methyladenosine (mA) modification stands out among various RNA modifications as the predominant form within eukaryotic cells, influencing numerous cellular processes implicated in disease development. mA modification has gained increasing attention in the development of atherosclerosis and has become a research hotspot in recent years. Programmed cell death (PCD), encompassing apoptosis, autophagy, pyroptosis, ferroptosis, and necroptosis, plays a pivotal role in atherosclerosis pathogenesis. In this review, we delve into the intricate interplay between mA modification and diverse PCD pathways, shedding light on their complex association during the onset and progression of atherosclerosis. Clarifying the relationship between mA and PCD in atherosclerosis is of great significance to provide novel strategies for cardiovascular disease treatment.
N6-甲基腺苷(mA)修饰在各种 RNA 修饰中脱颖而出,是真核细胞内的主要形式,影响着许多与疾病发展有关的细胞过程。mA 修饰在动脉粥样硬化的发展中受到越来越多的关注,近年来已成为研究热点。程序性细胞死亡(PCD)包括细胞凋亡、自噬、细胞焦亡、铁死亡和坏死性凋亡,在动脉粥样硬化发病机制中起着关键作用。在这篇综述中,我们深入探讨了 mA 修饰与多种 PCD 途径之间的复杂相互作用,阐明了它们在动脉粥样硬化发生和进展过程中的复杂关系。阐明 mA 与动脉粥样硬化中 PCD 的关系对于为心血管疾病治疗提供新策略具有重要意义。