The Aging Arterial Wall

A chronic increase in the production of inflammatory signals drives age-associated arterial structural remodeling and functional changes, including diffuse arterial intimal-medial thickening and stiffening. Under the microscope, the aged artery is characterized by increases in vascular smooth muscle cell apoptosis, senescence, invasion, proliferation, inflammatory molecule secretion, endothelial disruption, prothrombosis, glycoxidation, fibrosis, elastin fragmentation, calcification, and amyloidosis. These adverse cellular and molecular events occur within aged arterial wall experimentally in young animals under inflammatory stress conditions, and are attenuated in old animals by interfering with proinflammatory signals. Importantly, the profile of arterial aging is intertwined with hypertension and atherosclerosis at the molecular, cellular, vascular, and clinical levels, rendering the aged arterial wall a fertile soil for their pathogenesis. Thus, early and effective strategies to suppress age-associated arterial proinflammation may be realistic approaches to curb the initiation and progression of age-associated cardiovascular diseases such as hypertension and atherosclerosis.