机制(生物学)
甲基转移酶
疾病
生物
调解人
化学
调解
糖尿病
蛋白质亚单位
生物信息学
小RNA
核糖核酸
表观遗传学
脂毒性
炎症
细胞生物学
信使核糖核酸
端粒酶
2型糖尿病
端粒
细胞因子
下调和上调
肥胖
基因沉默
甲基化
脂肪细胞
癌症研究
白细胞介素6
西妥因1
基因表达调控
信号转导
酶
作者
Li-Bao Cui,Jun Wang,Yan Ying,Heng‐Rong Fang
标识
DOI:10.1016/j.phrs.2025.107962
摘要
Metabolism-related diseases, including obesity, non-alcoholic fatty liver disease (NAFLD), Atherosclerosis (As),type 2 diabetes mellitus (T2DM), and diabetic complications, are rising at an alarming rate globally, significantly increasing the risk of life-threatening conditions. Furthermore, these diseases have emerged as a major public health challenge worldwide. N6-methyladenosine (m6A) is the most abundant post-transcriptional modification in eukaryotic messenger RNA molecules, catalyzed by methyltransferase complexes, with methyltransferase-like 3 (METTL3) serving as the sole catalytic subunit due to its unique structural properties. As a critical component of the m6A methylation mechanism, METTL3 profoundly influences metabolism-related diseases through various pathways, including the regulation of adipocyte differentiation, modulation of key metabolic genes, and mediation of inflammatory responses via cytokine secretion. This article reviews recent research findings that elucidate the precise molecular mechanisms underlying METTL3's involvement in these processes and assesses its potential as a therapeutic target, along with the associated challenges.
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