运动改善T2DM代谢机制:AMPK通路与MSTN核心基因作用解析

2026-03-14 MedSci xAi 发表于广东省
本研究基于GSE205891和GSE230002数据集,识别出26个在运动干预T2DM中共同差异表达的核心基因,通过GO/KEGG分析揭示AMPK信号通路关键作用,PPI网络确定MSTN为核心调控节点,为运动改善糖尿病代谢提供分子机制证据。
From the dataset GSE205891, 81 differentially expressed genes (34 upregulated and 47 downregulated) were identified, and from the dataset GSE230002, 100 differentially expressed genes (41 upregulated and 59 downregulated) were identified. Among these, 26 genes were significantly differentially expressed in both datasets, suggesting that these genes may play a central role in the metabolic improvement of T2DM through exercise. Gene Ontology (GO) and KEGG pathway enrichment analyses were performed on the intersecting genes. The GO enrichment analysis revealed significant biological processes including skeletal muscle tissue development, cytokine response, and insulin response; cellular components were mainly focused on myofibrils and contractile myofibers; molecular functions primarily involved growth factor binding and cytokine activity. Notably, KEGG pathway analysis showed significant enrichment of the AMPK signaling pathway. A protein-protein interaction (PPI) network was constructed for the intersecting genes, and 10 hub genes, including MYH1, MYH4, and MSTN, were identified. Among these, MSTN is located at the core node of the PPI network and shows significant interactions with metabolic regulatory genes such as ACTN3 and LEP. MSTN, a common myokine, has received considerable attention in the context of exercise intervention for T2DM and is considered an important indicator for subsequent research.
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