Role of extracellular matrix in vascular remodeling of hypertension

Arterial stiffness due to alterations in extracellular matrix is one of the mechanisms responsible for increased peripheral resistance in hypertension. Recent evidence points to arterial stiffness as an independent predictor of cardiovascular events. This review focuses on recent advances in the biology of extracellular matrix proteins involved in hypertension-associated vascular changes.

The vascular extracellular matrix is a complex heterogeneous tissue comprising collagens, elastin, glycoproteins, and proteoglycans. These constituents not only provide mechanical integrity to the vessel wall but also possess a repertoire of insoluble ligands that induce cell signaling to control proliferation, migration, differentiation, and survival. It is now evident that it is not only the quantity but also the quality of the new synthesized extracellular matrix that determines changes in vascular stiffness in hypertension. Also, the control of cross-linking and the interactions between the extracellular matrix and vascular cells seem to be important.

It is now evident that some of the currently used antihypertensive therapies can correct vascular stiffness and fibrosis. A better understanding of molecular mechanisms underlying alterations in extracellular matrix in hypertension will provide insights into novel therapies to reduce arterial stiffness and will identify new roles of established antihypertensive drugs.