Background: Vascular smooth muscle cells (VSMCs) show eminently
plasticity during physiological and pathological processes. VSMCs undergo from
contractile phenotype to proliferative, matrigenic, inflammatory or osteogenic phenotype
during the pathogenesis of hypertension, atherosclerosis, and vascular calcification
Methods: Here we reviewed the research papers regarding to the respective effects of extracellular
matrix (ECM) on VSMC phenotypic switching.
Results: The ECM including collagens, elastins, proteoglycans and glycoproteins etc, via complex
protein-protein interaction, constitute a complicated microenvironment for VSMCs. Each component
regulates VSMC phenotypic switching via various signaling pathways and cell surface receptor.
On the other hand, ECM can be dynamic degraded or proteolysed by a variety of extracellular
proteinases such as matrix metalloproteinases (MMPs) and a disintegrin and metalloprotease with
thrombospondin motifs (ADAMTS). Thus, these extracellular proteinases are able to modulate
VSMC phenotypes partially via degrading ECM. Moreover, the ECM-modulated VSMC phenotypic
switching also plays a critical role in various vascular diseases, such as hypertension, atherosclerosis
and vascular calcification.
Conclusion: Various ECM compositions including fibrous proteins, glycoproteins and proteoglycans
exhibit the ability to modulate the VSMC phenotypic switching.