The regulatory role of m6A methylation modification in metabolic syndrome pathogenesis and progression

被引:1
|
作者
Ye, Diwen [1 ,2 ]
Zhang, Yongjiao [1 ,2 ]
Zhang, Bingyang [2 ]
Liu, Junjun [2 ]
Wei, Tianshu [2 ]
Lu, Sumei [1 ,2 ]
机构
[1] Shandong First Med Univ, Affiliated Hosp 1, Dept Lab Med, Jinan, Peoples R China
[2] Weifang Med Univ, Sch Med Lab, Weifang, Shandong, Peoples R China
关键词
m; 6; A; nonalcoholic fatty liver disease; diabetes; atherosclerosis; inflammatory response; autophagy; programmed cell death; metabolic syndrome; MESSENGER-RNA; TRANSLATION; EXPRESSION; AUTOPHAGY; OBESITY; APOPTOSIS;
D O I
10.3389/fphys.2024.1271874
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
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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页数:11
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