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. 2017 Dec 5;4(4):22. doi: 10.3390/jcdd4040022

Table 1.

Effects of EPAC1 on experimental neointimal hyperplasia.

Experimental Model Treatments Effects
Carotid arteries and vascular smooth muscle cells (VSMCs) from wild type (WT) and EPAC1 −/− mice. Ligation of carotid arteries and pharmacological inhibition of EPAC1 Neointima formation and VSMC proliferation were reduced in EPAC1 −/− mice. ESI09 also reduced neointima formation [60].
VSMCs from thoracic aorta explants from WT and EPAC1 −/− mice. Injury of femoral artery Reduced neointima formation and reduced migration of VSMCs in EPAC1 −/− mice [61].
Human saphenous vein VSMCs Effects of pharmacological EPAC activation on VSMC migration EPAC activation reduced VSMC migration and serum-induced vessel wall thickening [49].
Rat VSMCs from aorta explants. Phamacological activation of EPAC and PKA A combination of EPAC and PKA activation inhibited serum-induced VSMC proliferation [50].
VSMCs from foetal and adult rat aorta. Pharmacological activation of EPAC and adenovirus-mediated overexpression of EPAC1 EPAC activation and overexpression of EPAC1 enhanced intimal thickening in aorta and VSMC proliferation [62].
Primary aortic VSMCs from male rats Pharmacological activation of EPAC and PKA PKA and EPAC work cooperatively to inhibit VSMC migration [63].