Table 1.

Table representing the expression of different integrin subunits, their implication in smooth muscle cell (SMC) function and disease conditions such as atherosclerosis and neointimal hyperplasia, and integrin-directed drugs used in clinics. Collagen, Col; Laminin, LN; Fibronectin, Fn; Vascular cell adhesion molecule, VCAM; Osteopontin, OPN; Tenascin, TN; Vitronectin, VN; Fibrinogen, Fib; EDA, extra domain A.

Integrin	ECM	SMC Expression	SMC Function	Implication in Atherosclerosis/Restenosis	Integrin-Targeting Agents in Clinics	Reference
α1β1	Col 1-IV, LN	High expression in resting SMCs. Downregulated in culture conditions and during neointimal hyperplasia	Promotes SMC adhesion and contractile phenotype	α1β1 deletion induces a stable plaque phenotype	SAN-300	[10,34,42,52,53,54,55]
α2β1	Col 1 and IV, LN	Undetectable levels in normal human SMCs, and high expression in cultured SMCs	promote chemotaxis of arterial SMCs	α2β1 deletion had no effect on atherosclerosis	Vatelizu-mab	[16,39,42,52,56]
α3β1	Col 1, Fn, and LN	Detectable levels in normal human SMCs, and high expression in cultured SMCs	No conclusive reports			[10,33]
α4β1	Cellular-Fn, VCAM, OPN	Undetectable levels in normal human SMCs, expressed in SMCs in culture and in intimal atherosclerotic thickening	Induction of SMC differentiation	blocking α4β1 prevents neointimal hyperplasia	Natalizu-mab AJM300	[38,44,45,52]
α5β1	Fn and LN	Low levels in normal human SMCs, and high expression in cultured SMCs and during neointimal hyperplasia	Promote SMC proliferation and migration	Mediates early atherosclerosis	Volocixi-mab ATN61	[41,57,58]
α7β1	LN	High levels in normal SMCs, and low expression in synthetic SMC	Promotes contractile SMC phenotype	α7 deletion promotes neointimal hyperplasia	No conclusive reports	[20,51,59,60]
α8β1	Fn, TN, VN	Overexpressed in SMCs that display a contractile phenotype low expression in synthetic SMC phenotype and during neointimal hyperplasia	Promotes contractile SMC phenotype. Prevents SMC proliferation and migration	α8 deletion aggravates intimal thickening	No conclusive reports	[12,35,50,61]
α9β1	Fn-EDA, TN, VCAM	Expression increases in synthetic SMC phenotype	Promotes SMC proliferation, migration, and synthetic phenotype.	α9 deletion prevents NH	ASP5094	[21,62]
αvβ1	VN, Fn	Weakly expressed in normal SMCs, and upregulated in SMCs cultured on fibronectin	Inhibits contractility in SMC exposed to serum	No conclusive reports	PLN-74809 PLN-1474	[41,63,64]
αvβ3	VN, OPN, Fn	Weakly expressed in normal SMCs, and upregulated in SMCs cultured on fibronectin and during neointimal hyperplasia	Promotes SMC adhesion, proliferation and migration	Promotes neointimal hyperplasia	LM609, Abcixi-mab (c7E3Fab; ReoPro), Vitaxin, Intetumu-mab, Cillengitide	[16,41,65,66,67,68]
αvβ5	Fib, Fn, OPN VN	highly abundant in cultured SMCs, upregulated upon vascular injury	Promotes SMC adhesion and migration	Promotes neointimal hyperplasia	LM609 Intetumu-mab	[67,69]