Interaction between insulin-like growth factor-1 and atherosclerosis and vascular aging.

摘要: The process of vascular aging encompasses alterations in the function endothelial (ECs) and smooth muscle cells (VSMCs) via oxidation, inflammation, cell senescence epigenetic modifications, increasing probability atherosclerosis. Aged vessels exhibit decreased antithrombogenic properties, increased reactive oxygen species generation, inflammatory signaling migration VSMCs to subintimal space, impaired angiogenesis elastin degradation. key initiating step atherogenesis is subendothelial accumulation apolipoprotein B-containing low-density lipoproteins resulting activation ECs recruitment monocytes. Activated secrete 'chemokines' that interact with cognate chemokine receptors on monocytes promote directional migration. Recruitment immune establishes a proinflammatory status, further causing elevated oxidative stress, which turn triggers series events including apoptotic or necrotic death nonvascular cells. Increased stress also considered be factor mechanisms aging-associated changes tissue integrity function. Experimental evidence indicates insulin-like growth factor-1 exerts antioxidant, anti-inflammatory pro-survival effects vasculature, reducing atherosclerotic plaque burden promoting features stability.