Abstract
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.