Department of Cardiology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China.
Department of Cardiology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200092, China.
Int J Cardiol. 2022 Nov 15;367:11-19. doi: 10.1016/j.ijcard.2022.08.042. Epub 2022 Aug 21.
N(6)-methyladenosine (mA) modification is closely associated with myocardial ischemia/reperfusion injury (MIRI). As the most common modification among RNA modifications, the reversible mA modification is processed by methylase ("writers") and demethylase ("erasers"). The biological effects of RNA modified by mA are regulated under the corresponding RNA binding proteins (RBPs) ("readers"). mA modification regulates the whole process of RNA, including transcription, processing, splicing, nuclear export, stability, degradation, and translation. Programmed cell death (PCD) is a regulated mechanism that maintains the internal environment's stability. PCD plays an essential role in MIRI, including apoptosis, autophagy, pyroptosis, ferroptosis, and necroptosis. However, the relationship between PCD modified with mA and MIRI is still not clear. This review summarizes the regulators of mA modification and their bioeffects on PCD in MIRI.
N(6)-甲基腺苷(m6A)修饰与心肌缺血/再灌注损伤(MIRI)密切相关。作为 RNA 修饰中最常见的修饰,可逆的 m6A 修饰由甲基转移酶(“写入器”)和去甲基化酶(“橡皮擦”)处理。受 m6A 修饰的 RNA 的生物学效应受相应的 RNA 结合蛋白(RBPs)(“读取器”)调节。m6A 修饰调节 RNA 的全过程,包括转录、加工、剪接、核输出、稳定性、降解和翻译。程序性细胞死亡(PCD)是一种维持内部环境稳定的调节机制。PCD 在 MIRI 中发挥着重要作用,包括细胞凋亡、自噬、细胞焦亡、铁死亡和坏死性凋亡。然而,m6A 修饰的 PCD 与 MIRI 之间的关系尚不清楚。本综述总结了 m6A 修饰的调节剂及其在 MIRI 中对 PCD 的生物效应。