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M6a甲基化:控制2型糖尿病及其并发症发展的新途径。

M6a Methylation: A New Avenue for Control of the Development of Type 2 Diabetes Mellitus and its Complications.

作者信息

Liu Chunyan, Na Lixin

机构信息

College of Public Health, Shanghai University of Medicine and Health Sciences, Shanghai, China.

出版信息

Endocr Metab Immune Disord Drug Targets. 2024 Aug 22. doi: 10.2174/0118715303320146240816113924.

Abstract

The rapidly emerging prevalence of type 2 diabetes mellitus (T2DM) and its associated complications have formed an increasingly serious threat to human life and health. Therefore, there is an urgent requirement to investigate the pathogenesis of T2DM and its complications, which will be conducive to discovering effective drugs for prevention and treatment. N6-methyladenosine (m6A) methylation is the most abundant and prevalent epigenetic modification of mRNA in mammals. m6A methylation is a dynamically reversible epigenetic transcriptome modification process that is jointly regulated by methyltransferases, demethylases and methylated reading proteins, which control the fate of target mRNAs through influencing splicing, translation and decay. Recent studies have revealed that m6A methylation plays an important role in β cellular function, insulin sensitivity and glycolipid metabolism. In this review, we summarized the current roles of m6A methylation in T2DM and T2DM-related complications such as diabetes nephropathy (DN), diabetes cardiovascular disease (DCD) and diabetes retinopathy (DR). Additionally, we sought the potential mechanism of m6A in T2DM and related complications, which may provide a rationale and strategy for potential therapeutic targeting of T2DM and its complications.

摘要

2型糖尿病(T2DM)及其相关并发症的迅速流行对人类生命和健康构成了日益严重的威胁。因此,迫切需要研究T2DM及其并发症的发病机制,这将有助于发现预防和治疗的有效药物。N6-甲基腺苷(m6A)甲基化是哺乳动物中mRNA最丰富、最普遍的表观遗传修饰。m6A甲基化是一个动态可逆的表观转录组修饰过程,由甲基转移酶、去甲基酶和甲基化阅读蛋白共同调控,它们通过影响剪接、翻译和降解来控制靶mRNA的命运。最近的研究表明,m6A甲基化在β细胞功能、胰岛素敏感性和糖脂代谢中起重要作用。在这篇综述中,我们总结了m6A甲基化在T2DM和T2DM相关并发症如糖尿病肾病(DN)、糖尿病心血管疾病(DCD)和糖尿病视网膜病变(DR)中的当前作用。此外,我们探讨了m6A在T2DM及其相关并发症中的潜在机制,这可能为T2DM及其并发症的潜在治疗靶点提供理论依据和策略。

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