抑郁症的病因复杂，包括遗传因素、生物学因素和心理社会因素等多种因素。RNA甲基化及其相关的下游信号通路影响着多种生物机制，包括细胞分化、肿瘤发生、性别决定和应激反应。本研究通过搜索PubMed、Web of Science、国家科学技术图书馆（NSTL）和ScienceDirect Online（SDOL）数据库，总结了RNA甲基化在抑郁症病理机制中的生物学作用。RNA甲基化在多种疾病的发展中发挥着关键作用，目前的研究显示RNA甲基化与抑郁症密切相关。抑郁症中的RNA甲基化主要涉及“写手”（介导RNA的甲基化修饰过程）和“擦除剂”（介导RNA甲基化的去甲基化修饰过程）。肥胖相关基因（FTO）通过增加体质量指数（BMI）、降低多巴胺水平、抑制肾上腺素β2受体（ADRB2）-c-Myc-sirt1通路，导致大脑中m6A/m6Am调控失常，可能参与了抑郁症的发病机制。研究RNA甲基化在抑郁症中的作用进一步加深了我们对抑郁症病理发生机制和发展过程的认识，为抑郁症病理机制的研究提供了新的视角，并为该疾病的预防和治疗提供了新的靶点。版权所有 © 2023。Elsevier Inc.出版。

Depression is caused by a variety of factors such as genetic factors, biological factors, and psychosocial factors, and the pathogenesis is complex. RNA methylations and related downstream signaling pathways influence a variety of biological mechanisms, including cell differentiation, tumorigenesis, sex determination, and stress response. In this work, we searched the PubMed, Web of Science, National Library of Science and Technology (NSTL), and ScienceDirect Online (SDOL) databases to summarize the biological roles of RNA methylations and their impact on the pathological mechanisms of depression. RNA methylations play a key role in the development of many diseases, and current research shows that RNA methylations are also closely linked to depression. RNA methylations in depression mainly involve "writers" (mediating the methylation modification process of RNAs), "erasers" (mediating the demethylation modification process of RNA methylation). Fat Mass and Obesity Associated (FTO) influences the development of depression by increasing body mass index (BMI), decreases the dopamine level, inhibits the adrenoceptor beta 2 (ADRB2)-c-Myc-sirt1 pathway, results in the m6A/m6Am dysregulation in brain, and may be involved in the pathogenesis of depression. The study of RNA methylations in depression has further deepened our understanding of the pathogenesis and development process of depression, provides new perspectives for the study of the pathological mechanism of depression, and provides new targets for the prevention and treatment of this disease.Copyright © 2023. Published by Elsevier Inc.