Li Rongxian, Wu Chaojie, Zhao Yuan, Jiang Shiyi, Huang Junben, Huo Xiuyun, Deng Chang, He Zuoshun, Gu Shiyan, Yang Jie
School of Public Health, Dali University, Dali, Yunnan, China.
Institute of Preventive Medicine, Dali University, Dali, Yunnan, China.
Heliyon. 2024 Nov 17;10(22):e40473. doi: 10.1016/j.heliyon.2024.e40473. eCollection 2024 Nov 30.
Arsenic can cause extensive toxic damage after entering the body of humans and animals by altering a variety of events. As the most common form of methylation modification of RNA in eukaryotic cells, N-methyladenosine (mA) is widely involved in regulating RNA processing, translation and degradation, thus playing important role in various pathophysiological processes. Emerging studies have demonstrated that mA modification is synergistically mediated by methyltransferases, demethylases and methyl-binding proteins. Recently, emerging studies have shown that mA modification and its regulatory proteins play important roles in arsenic toxicity through mediating various key signaling pathways. We comprehensively analyzed the mechanisms by which mA modification and its regulatory proteins contribute to arsenic toxicity. Our reviews offer a scientific foundation for the development of preventive and control strategies to mitigate arsenic-induced toxicity, with an emphasis on an epigenetic approach.
砷进入人和动物体内后,可通过改变多种生理过程造成广泛的毒性损害。作为真核细胞中RNA最常见的甲基化修饰形式,N-甲基腺苷(mA)广泛参与调节RNA加工、翻译及降解,进而在各种病理生理过程中发挥重要作用。新兴研究表明,mA修饰由甲基转移酶、去甲基酶和甲基结合蛋白协同介导。最近,新兴研究显示,mA修饰及其调控蛋白通过介导各种关键信号通路在砷毒性中发挥重要作用。我们全面分析了mA修饰及其调控蛋白导致砷毒性的机制。我们的综述为制定预防和控制策略以减轻砷诱导的毒性提供了科学依据,重点是表观遗传学方法。