Hao Xiaoyu, Tu Siying, Pan Da, Liao Wang, Yang Ligang, Wang Shaokang, Sun Guiju
Key Laboratory of Environmental Medicine and Engineering of Ministry of Education, Department of Nutrition and Food Hygiene, School of Public Health, Southeast University, Nanjing 210009, China.
Clinical Medical Research Center for Plateau Gastroenterological Disease of Xizang Autonomous Region, School of Medicine, Xizang Minzu University, Xianyang 712082, China.
Metabolites. 2025 Sep 15;15(9):613. doi: 10.3390/metabo15090613.
Ageing drives a vicious cycle of insulin resistance (IR) and atherosclerosis through shared pathological pathways. This review aims to synthesise the current understanding of the molecular mechanisms that connect ageing, IR, and atherosclerosis, with a particular focus on oxidative stress, chronic inflammation, and metabolic disturbances. We systematically summarise evidence demonstrating how age-related mitochondrial dysfunction promotes IR, which in turn accelerates atherosclerotic progression. Based on this integration, we conclude that the intertwined nature of these processes reveals promising therapeutic targets. Targeting these shared pathways, such as with senolytic agents or anti-inflammatory agents, may offer novel strategic insights for concurrently mitigating IR and atherosclerosis in the ageing population.
衰老通过共同的病理途径驱动胰岛素抵抗（IR）和动脉粥样硬化的恶性循环。本综述旨在综合当前对连接衰老、IR和动脉粥样硬化的分子机制的理解，特别关注氧化应激、慢性炎症和代谢紊乱。我们系统地总结了证据，证明与年龄相关的线粒体功能障碍如何促进IR，而IR又反过来加速动脉粥样硬化的进展。基于这种整合，我们得出结论，这些过程的相互交织性质揭示了有前景的治疗靶点。针对这些共同途径，如使用衰老细胞溶解剂或抗炎剂，可能为同时减轻老年人群中的IR和动脉粥样硬化提供新的战略见解。
