Review reveals m6A modification impacts obesity through metabolic pathways, suggesting therapeutic potential.
Obesity has emerged as a global health challenge, closely associated with multiple metabolic diseases, such as cardiovascular diseases, type 2 diabetes, and non-alcoholic fatty liver disease. The traditional “calories-in minus calories-out” paradigm is no longer sufficient to explain the heterogeneity of obesity; consequently, a growing body of research has turned its focus to epigenetic regulation—particularly chemical modifications at the RNA level. N6-methyladenosine (m6A) modification is one of the most abundant epigenetic modifications on RNA, which dynamically regulates the methylation reaction in specific sequences on mRNA through methyltransferases (writers), demethylases (erasers), and binding proteins (readers). Accumulating evidence in recent years has revealed that m6A modification plays a pivotal role in the pathogenesis and progression of obesity, particularly through its regulation of key biological processes, such as adipocyte differentiation, lipid metabolism, and energy homeostasis. Given its critical involvement in metabolic dysregulation, targeting m6A-related mechanisms may offer novel therapeutic avenues for obesity management. This review systematically summarizes the current understanding of m6A modification in obesity, elucidates its underlying molecular mechanisms, and evaluates its potential as a therapeutic target. By integrating recent advances in the field, we aim to provide new perspectives for the development of innovative strategies in obesity treatment.
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Chen et al. (2025) studied this question.
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