Table 2.

Experimental models of the effects of RA on the migration of VSMCs.

First Author (Year)	Experimental Model	Agent, Dose of Administration	Main Results	Other Results
Kato S. (1993) [48]	human aortic SMCs		• Downregulation of the production of proMMP-1 after treatment with PDGF
Axel D. (2000) [16]	mono- and transfilter co-cultures of human arteries SMC	0.01 nM–10.0 mM atRA	• Migration and proliferation inhibition through reduction in MMP-2 and MMP-9 expression	• Decrease in mRNA expression of the glycoproteins thrombospondin-1, fibronectin
Suganuma E. (2021) [49]	Male mouse model of Kawasaki disease	30 mg/kg ATRA, oral administration	• Reduction in elastin break score of external and internal elastin lumina • Suppression of MMP-9 protein	• Lower coronary stenosis and inflammatory scores • Augmentation of their area coverage by migration cells after stimulation by platelet-derived PDGF-BB
Johst U. (2003) [50]	human aortic SMC	10−6 M, 10−7 M, and 10−8 M ATRA, 9cis RA	• Decrease in migrated cells associated with reduced production of tenascin and downregulation of p44/p42 MAPKs	• Increased G1-phase • Stronger expression of α-actin
Neuville P. (1999) [29]	Cultured aortic media and intimal thickening rat SMC, angioplasty of rat carotid artery and thoracic aorta	10−6 final concentration, 0.5 mg/kg intraperitoneally/day for 14 days of RA	• Increased migration and tissue-type plasminogen activator activity	• Reduced the intimal hyperplasia in the carotid artery in vivo

MAPKs: mitogen-activated protein kinases, MMP 2: matrix metalloproteinase-2, MMP 9: matrix metalloproteinase 9, PDGF: platelet-derived growth factor, PDGF-BB: platelet-derived growth factor-BB.