517-肥胖通过损害SAMHD1引发炎症机制研究

这项研究揭示了肥胖导致慢性炎症的分子机制，重点关注NLRP3炎性小体的过度激活。研究发现，肥胖会改变巨噬细胞的核苷酸代谢，使其从正常的线粒体合成途径转向直接从胞质导入dNTP。这种代谢重编程受SAMHD1蛋白失活的驱动，导致线粒体内的DNA含量增加并产生氧化mtDNA。这些受损的遗传物质释放到胞质后，会诱发严重的炎症反应并加剧胰岛素抵抗及脂肪肝等代谢疾病。通过抑制相关的转运蛋白或恢复代谢平衡，有望成为治疗肥胖相关炎症的新策略。因此，该成果为缓解肥胖引起的非传染性疾病提供了潜在的治疗靶点。References: Liu D, Zhou C, Wang X, et al. Nucleotide metabolic rewiring enables NLRP3 inflammasome hyperactivation in obesity[J]. Science, 2026, 391(6782): eadq9006.前往小宇宙评论区与主播互动

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517-肥胖通过损害SAMHD1引发炎症机制研究

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