Qin Cong, Qin Yansong, Zhou Shanshan
Department of Cardiology, The First Hospital of Jilin University, Changchun, China.
Undergraduate School, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Front Cardiovasc Med. 2025 Apr 11;12:1559550. doi: 10.3389/fcvm.2025.1559550. eCollection 2025.
Dilated cardiomyopathy (DCM) is characterized by impaired expansion or contraction of the left or both ventricles in the absence of abnormal load conditions (such as primary valve disease) or severe coronary artery disease that can lead to ventricular remodeling. Genetic mutations, infections, inflammation, autoimmune diseases, exposure to toxins, and endocrine or neuromuscular factors have all been implicated in the causation of DCM. Cardiomyopathy, particularly DCM, often has genetic underpinnings, with established or suspected genetic origins. Up to 40% of DCM cases involve probable or confirmed genetic variations. The significance of RNA modification in the pathogenesis of hypertension, cardiac hypertrophy, and atherosclerosis is well-established. Of late, RNA methylation has garnered attention for its involvement in DCM. This review examines the biological mechanisms and effects of RNA methylation in DCM and heart failure.
扩张型心肌病（DCM）的特征是在没有异常负荷情况（如原发性瓣膜病）或可导致心室重构的严重冠状动脉疾病的情况下，左心室或双心室的舒张或收缩功能受损。基因突变、感染、炎症、自身免疫性疾病、接触毒素以及内分泌或神经肌肉因素均与DCM的病因有关。心肌病，尤其是DCM，通常具有遗传基础，有已确定或疑似的遗传起源。高达40%的DCM病例涉及可能或已证实的基因变异。RNA修饰在高血压、心脏肥大和动脉粥样硬化发病机制中的重要性已得到充分证实。最近，RNA甲基化因其与DCM的关系而受到关注。本综述探讨了RNA甲基化在DCM和心力衰竭中的生物学机制及作用。
