The regulatory role of m(6)A methylation modification in metabolic syndrome pathogenesis and progression

m(6)A甲基化修饰在代谢综合征发病机制和进展中的调控作用

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Abstract

Metabolic syndromes are characterized by various complications caused by disrupted glucose and lipid metabolism, which are major factors affecting the health of a population. However, existing diagnostic and treatment strategies have limitations, such as the lack of early diagnostic and therapeutic approaches, variability in patient responses to treatment, and cost-effectiveness. Therefore, developing alternative solutions for metabolic syndromes is crucial. N6-methyladenosine (m(6)A) is one of the most abundant modifications that determine the fate of RNA. m(6)A modifications are closely associated with metabolic syndrome development and present novel prospects for clinical applications. Aberrant m(6)A modifications have been detected during inflammatory infiltration, apoptosis, autophagy, iron sagging, necrosis, and scorching during metabolic syndrome pathogenesis and progression. However, few reviews have systematically described the correlation between m(6)A modifications and these factors concerning metabolic syndrome pathogenesis and progression. This study summarizes the m(6)A methylation regulators and their roles in metabolic syndrome development, highlighting the potential of m(6)A modification as a biomarker in metabolic disorders.

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