Table 2 Summary of structural, dynamic and external pathophysiological mechanisms characterized in arterial stiffness
Structural component: Arterial wall remodeling | Impaired collagen-elastin ratio | Type I collagen fibers increase and the number of elastic fibers and VSMC decrease, primarily by overstimulation of elastase and reduction of tropoelastin expression. |
Blood vessel calcification | Inflammation, oxidative stress, and the presence of cardiometabolic comorbidities decrease mitophagy and autophagy, and stimulate vascular calcification, which decreases vascular distensibility. | |
Endothelial dysfunction | Inflammation can cause disruptions in the regulation of vascular tone, leading to vascular dysfunction and irreversible vessel damage. | |
Increased intima-media thickness | Caused by VSMC migration, endothelial dysfunction, vascular calcification, increased activity of metalloproteinases, ECM degradation, oxidative stress, collagen and elastin degradation. | |
Dynamic component: Stress | Proinflammatory markers | Inflammation promotes activation of RAAS, the sympathetic nervous system and expression of endothelin-1, which leads to overproduction and increased secretion of MCP-1, TGF-β, matrix metalloproteinases, calpain-1, and MFG-E8, leading to age-associated arterial secretory phenotypes. |
Reactive oxygen species | Caused by increases in the production of ROS and in the expression of NADPH in the arterial wall, as well as a negative regulation of antioxidant proteins during vascular aging, such as superoxide dismutase. | |
Nitric Oxide | NO works as a regulator for vasodilation, stiffening and proinflammation. Decreases in NO synthase and NO concentrations in the arterial wall induce a proinflammatory reaction, generating ROS and increasing vasoconstriction. | |
External components | • Clinical risk factors (T2D, systemic arterial hypertension, obesity). • Genetic determinants. • Behavioral risk factors (smoking, alcoholism). | |
