Journal
CELLS
Volume 11, Issue 4, Pages -Publisher
MDPI
DOI: 10.3390/cells11040646
Keywords
integrins; smooth muscle cell; phenotype switching; neointimal hyperplasia; restenosis; extracellular matrix; fibronectin
Categories
Funding
- Department of Biotechnology, Government of India [BT/RLF/Re-entry/28/2019]
- National Institutes of Health [R35HL139926, R01NS109910, U01NS113388]
- American Heart Association [18EIA33900009]
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Integrins play a crucial role in modulating the functional properties of smooth muscle cells and their implications in vascular pathology.
Smooth muscle cells (SMCs), present in the media layer of blood vessels, are crucial in maintaining vascular homeostasis. Upon vascular injury, SMCs show a high degree of plasticity, undergo a change from a contractile to a synthetic phenotype, and play an essential role in the pathophysiology of diseases including atherosclerosis and restenosis. Integrins are cell surface receptors, which are involved in cell-to-cell binding and cell-to-extracellular-matrix interactions. By binding to extracellular matrix components, integrins trigger intracellular signaling and regulate several of the SMC function, including proliferation, migration, and phenotypic switching. Although pharmacological approaches, including antibodies and synthetic peptides, have been effectively utilized to target integrins to limit atherosclerosis and restenosis, none has been commercialized yet. A clear understanding of how integrins modulate SMC biology is essential to facilitate the development of integrin-based interventions to combat atherosclerosis and restenosis. Herein, we highlight the importance of integrins in modulating functional properties of SMCs and their implications for vascular pathology.
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