References | Animal models or cell types | Statins studied | Effects of statins | |||||||
Cx expression and gap junction |
| Improvement of pathological changes | ||||||||
Part 1: Modulation of Cxs/gap junctions by statins against atherosclerosis and neointimal hyperplasia | ||||||||||
[25] | rabbits fed with high-cholesterol diet | lovastatin, fluvastatin | expressions of Cx43 and Cx |
| neointima decreased in atherosclerotic lesions | |||||
[29] | LDLR−/− mice fed with cholesterol-rich diet | pravastatin | Cx43 expression reduced in lesions |
| improvement of plaque morphology and stability | |||||
cultured SMCs isolated from human saphenous veins | simvastatin | Cx43 expression reduced, reduced transfer of gap junction-permeable dye |
| ND | ||||||
[32] | rabbits fed with high-cholesterol diet | vytorin (simvastatin/ ezetimebe) | Cx43 expression reduced in aortic walls |
| neointimal hyperplasia and inflammatory cell infiltration reduced in lesions | |||||
cultured rat aortic SMCs, stimulated with or without TNF-α/IL-18 | simvastatin | Cx43 expression reduced (constitutive level as well as increased expression induced by TNF-α/IL-18) |
| over-proliferation of SMCs suppressed | ||||||
[27] | rabbits, arteries subjected to balloon injury | lovastatin, fluvastatin | expressions of Cx43 and Cx40 reduced in neointimal SMCs, volume and size of gap junctions reduced |
| neointima decreased | |||||
[33] | ex vivo cultured human saphenous veins | fluvastatin | expression of Cx43 reduced in neointimal SMCs |
| neointima decreased | |||||
[34] | cultured rat aortic SMCs | lovastatin | GJIC inhibited between SMCs |
| migration of SMCs inhibited | |||||
[35] | cultured SMCs isolated from human saphenous veins | atorvastatin controlled release from hydrogel | expression of Cx43 reduced |
| proliferation and migration of SMCs inhibited | |||||
[37] | rat diabetes induced by STZ injection | simvastatin | reversed the down-regulation of Cx |
| ND | |||||
[39] | hereditary HTG rats | atorvastatin | Cx43 expression reduced in aorta, distribution of Cx43 modified between endothelium and media |
| integrity of endothelium improved | |||||
[40] | cultured HUVEC | fluvastatin, lovastatin, pravastatin, simvastatin | statins reduced Cx43 expression when treated alone, but could reverse the down-regulating effect of nicotine on Cx43 |
| ND | |||||
[41] | mice hyperlipidemia induced by cholesterol-rich diet | simvastatin | reversed the reduction of Cx37 and gap junctions in aortic endothelium |
| ND | |||||
[42] | STZ induced diabetes in ApoE-deficient mice | simvastatin | exacerbated the reduction of Cx37 and Cx |
| - | |||||
Part 2: Modulation of Cxs/gap junctions by statins against arrhythmia and myocardial injury/hypertrophy | ||||||||||
[48] | hereditary HTG rats | atorvastatin | Cx43 expression increased, phosphorylation normalized; gap junction remodeling suppressed, integrity improved in ventricles |
| threshold for electric-induced VF increased | |||||
[49] | rat acute MI induced by coronary artery ligation | pravastatin | Cx43 expression increased, gap junction remodeling suppressed |
| incidence of VT/VF decreased | |||||
[50] [51] | mice viral myocarditis induced by CVB3 | atorvastatin, pravastatin | restored the reduction of Cx43 and Cx |
| myocardial inflammatory cell infiltration and necrosis decreased, animal survival rate increased | |||||