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REVIEW article
Front. Cardiovasc. Med.
Sec. General Cardiovascular Medicine
Volume 12 - 2025 | doi: 10.3389/fcvm.2025.1559550
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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.
Keywords: dilated cardiomyopathy, Methylation, cardiac hypertrophy, Heart Failure, M6A
Received: 13 Jan 2025; Accepted: 28 Mar 2025.
Copyright: © 2025 Qin, Qin and Zhou. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Shanshan Zhou, The First Hospital of Jilin University, Changchun, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.
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