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Structural support and mechanical properties of the vessel wall are conferred primarily by collagen and elastin, which form an organized extracellular matrix in the vessel's tunica media and adventitia. Collagen provides tensile strength at higher pressures, limiting distension, while elastin enables the vessel to stretch and recoil during the cardiac cycle. These proteins interact with smooth muscle cells and other ECM components to maintain vessel integrity, allow pulsatile blood flow, limit rupture risk, and provide the elasticity needed for healthy cardiovascular function. Aging, genetic disorders, or pathological remodeling of these matrix proteins disrupt the vessel's mechanical properties and contribute to cardiovascular disease[1][2][3][5][7].
Inhibition or stimulation of ECM production (fibrosis-modifying); Protection against ECM degradation; Modulation of cross-linking (e.g., for elastin/collagen)
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