坏死性下垂
上睑下垂
自噬
程序性细胞死亡
发病机制
细胞凋亡
生物
疾病
N6-甲基腺苷
死因
核糖核酸
细胞
细胞生物学
癌症研究
医学
免疫学
病理
遗传学
基因
甲基转移酶
甲基化
作者
Haijiao Long,Yulu Yu,Jie Ouyang,Hongwei Lu,Guo-Jun Zhao
标识
DOI:10.1186/s10020-024-00901-z
摘要
Abstract N6-methyladenosine (m 6 A) modification stands out among various RNA modifications as the predominant form within eukaryotic cells, influencing numerous cellular processes implicated in disease development. m 6 A 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 m 6 A modification and diverse PCD pathways, shedding light on their complex association during the onset and progression of atherosclerosis. Clarifying the relationship between m 6 A and PCD in atherosclerosis is of great significance to provide novel strategies for cardiovascular disease treatment.
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