Effects of Cerivastatin on Human Arterial Smooth Muscle Cell Proliferation and Migration in Transfilter Cocultures

Axel, Dorothea I.; Riessen, Reimer; Runge, Heike; Viebahn, Richard; Karsch, Karl R.

doi:10.1097/00005344-200004000-00016

Cited by 67 publications

(46 citation statements)

References 48 publications

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“…The inhibitory effects of mevastatin on ovarian cell proliferation are consistent with previous reports regarding other mesenchymal cell types, including vascular smooth muscle [141][142][143] , cardiomyocytes 144 , and mesangial cells 145 .…”

Section: Evidence For Statin Actions In Vitrosupporting

confidence: 90%

Statins in the Treatment of Polycystic Ovary Syndrome

Kodaman

Dulęba²

2008

Semin Reprod Med

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Many women of reproductive age are affected by polycystic ovary syndrome (PCOS), a heterogeneous endocrinopathy characterized by androgen excess, chronic oligo-anovulation and/or polycystic ovarian morphology. In addition, PCOS is often associated with insulin resistance, systemic inflammation and oxidative stress which, on one hand, lead to endothelial dysfunction and dyslipidemia with subsequent cardiovascular sequelae and, on the other hand, to hyperplasia of the ovarian theca compartment with resultant hyperandrogenism and anovulation. While traditionally statins have been used to treat dyslipidemia by blocking HMG-CoA reductase, the rate limiting step in cholesterol biosynthesis; in fact, they possess pleiotropic actions, resulting in antioxidant, antiinflammatory and anti-proliferative effects. Statins offer a novel therapeutic approach to PCOS in that they address the dyslipidemia associated with the syndrome, as well as hyperandrogenism/ hyperandrogenemia. These actions may be due to an inhibition of the effects of systemic inflammation and insulin resistance/hyperinsulinemia. Evidence to date, both in vitro and in vivo, suggests that statins have potential in the treatment of PCOS; however, further clinical trials are needed before they can be considered a standard of care in the medical management of this common endocrinopathy.

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Section: Evidence For Statin Actions In Vitrosupporting

confidence: 90%

Statins in the Treatment of Polycystic Ovary Syndrome

Kodaman

Dulęba²

2008

Semin Reprod Med

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“…Cerivastatin and simvastatin diminish the migration of unstimulated and growth-factor-activated vascular SMCs of arterial or venous origin in vitro as well as ex vivo. 52,53 Similar inhibitory functions apply to the proliferation of SMCs; however, interpretation of these data requires care, in view of the potential toxic, proapoptotic effects of HMG-CoA reductase inhibitors on these cells.…”

Section: In Vitro Studies Suggest Lipid-lowering-independent Antiinflmentioning

confidence: 99%

Inflammation, Immunity, and HMG-CoA Reductase Inhibitors

Schönbeck

Libby²

2004

Circulation

428

335

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Abstract-According to traditional thinking, atherosclerosis results from passive lipid deposition in the vascular wall.Thus, therapies predominantly targeted lipid metabolism. The contemporary view of atherosclerosis, however, has broadened to include an active and complex role for inflammation, orchestrated in part by mediators of the immune system. This recognition prompted the question of whether antiinflammatory interventions might provide a novel avenue for the treatment of atherosclerosis. Uncertainties about the type of antiinflammatory regimen and appropriate patient selection currently hamper clinical investigation. Yet cardiovascular scientists have begun to address these questions at the bench, in experimental models, and indirectly in humans. Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A HMG-CoA reductase (statins) have emerged as promising tools with dual functions. Originally designed to target elevated lipids, the "traditional" cause of atherosclerosis, statins might also confer cardiovascular benefit by directly or indirectly modulating the inflammatory component of this prevalent disease. Yet controversy persists regarding the (clinical) relevance of these potential non-LDL-lowering "pleiotropic" functions of statins. This overview addresses the controversy by reviewing in vitro and in vivo evidence regarding statins as antiinflammatory agents. Cardiovascular Benefits of Statins Beyond Lipid Lowering: Hints From Clinical TrialsIn 1994, the landmark Scandinavian Simvastatin Survival Study (4S) established the benefits of a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor (statin) on mortality in patients with atherosclerosis. 1 In accord with traditional acceptance of atherosclerosis as a consequence of lipid disorders, post-hoc analysis of the 4S trial suggested that the benefit provided by simvastatin in individual patients indeed related to the magnitude of change in low-density-lipoprotein cholesterol (LDL-C). 2 Subsequent studies, however, differed with this conclusion even as they affirmed the clinical benefits of statins as a class on cardiovascular (CV) morbidity and mortality in patients with or without established atherosclerotic disease. In one post-hoc analysis of the West of Scotland Coronary Prevention Study (WOSCOPS) population, the Framingham coronary heart disease model accurately predicted the risk in placebo-treated subjects but underestimated the CV benefit to the statintreated group predicted by the degree of LDL lowering. 3 In the Cholesterol and Recurrent Events (CARE) study, pravastatin-mediated lowering of cholesterol and triglycerides appeared to account for most but not all of the benefits, lending further support to the hypothesis that statins provide CV benefit beyond lipid lowering. 4 Indeed, analysis of the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) study, 5 the Long-Term Intervention with Pravastatin in Ischemic Disease (LIPID) trial, 6 and the Heart Protection Study (HPS) 7 suggested that treatment effects...

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“…Statins have been recognized to exhibit various protective effects against atherosclerosis, including improvement of endothelial function 35) , decreased inflammation 36) , and inhibition of VSMC proliferation and migration 37) , all of which cannot be accounted for by lipid-lowering effects. One interesting pleiotropic effect of statins may be the Results from clinical observational studies suggest an association of statin use with slowed progression of calcific aortic stenosis and coronary artery calcification [38][39][40][41] .…”

Section: Effect Of Statins On Vascular Calcificationmentioning

confidence: 99%

Mechanism of Pi-induced Vascular Calcification - Regulation of Growth Arrest-Specific Gene 6 (Gas6)-Mediated Survival Pathway

Son

Akishita

Iijima

et al. 2008

JAT

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Vascular calcification is clinically important in the development of cardiovascular disease. It has been suggested that apoptosis is one of the processes regulating calcification in vascular smooth muscle cells (VSMC). In this review, we discuss the role of apoptosis in inorganic phosphate (Pi)-induced calcification, focusing on regulation of the survival pathway mediated by growth arrest-specific gene 6 (Gas6). Further, we mention the beneficial effect of statins mediated by inhibition of apoptosis which is accompanied by restoration of the Gas6-mediated survival pathway. These findings indicate that Gas6 is a novel target of statins' effects to prevent vascular calcification.

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Effects of Cerivastatin on Human Arterial Smooth Muscle Cell Proliferation and Migration in Transfilter Cocultures

Cited by 67 publications

References 48 publications

Statins in the Treatment of Polycystic Ovary Syndrome

Statins in the Treatment of Polycystic Ovary Syndrome

Inflammation, Immunity, and HMG-CoA Reductase Inhibitors

Mechanism of Pi-induced Vascular Calcification - Regulation of Growth Arrest-Specific Gene 6 (Gas6)-Mediated Survival Pathway

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