3-Hydroxy-3-methylglutaryl coenzyme a (HMG-CoA) reductase inhibitors (statins), atherosclerosis and coronary syndromes

Blum, Arnon; Simsolo, Claudia; Hasin, Yonathan

doi:10.1016/j.atherosclerosis.2003.12.024

Cited by 13 publications

(10 citation statements)

References 17 publications

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“…6 When it comes to a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin), many studies have revealed prevention of restenosis by statin treatment. [7][8][9] On the other hand, Petronio et al 10 reported that a statin does not inhibit restenosis in normocholesterolemic patients undergoing coronary stenting.…”

Section: Introductionmentioning

confidence: 97%

Effects of Combined Treatment with Angiotensin II Type 1 Receptor Blocker and Statin on Stent Restenosis

Yasukawa

Nakamura²,

Nagase

et al. 2009

Journal of Cardiovascular Pharmacology

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Angiotensin II type I receptor blocker (ARB) or statin has been reported to be effective in preventing stent restenosis, but little is known about the combined effect on stent restenosis. The objective of this study was to determine the effect of combination therapy with ARB and statin on restenosis rate after coronary stenting and on proliferation and migration of and reactive oxygen species (ROS) production by human coronary artery smooth muscle cells (SMCs) in vitro. Clinical data were collected from 330 consecutive patients who underwent coronary stenting for de novo lesions. Six months after stenting, quantitative coronary angiography was performed. Combined therapy with the ARB and statin significantly inhibited stent restenosis (P < 0.05) compared with the effect of the ARB or statin alone. In an in vitro study, platelet-derived growth factor (PDGF)-induced proliferation was significantly inhibited by combined treatment with CV11974, an ARB, and simvastatin (P < 0.01), but the inhibitory effect was not significantly greater than that of simvastatin alone. Migration of human coronary artery SMCs was significantly inhibited by the ARB + statin compared with the effect of the ARB or statin alone (P < 0.01). PDGF-induced production of ROS was also inhibited significantly by the ARB + statin compared with the effect of the ARB or statin alone (P < 0.01). These results indicate that inhibitory effects of combined therapy on PDGF-induced migration of and ROS production by SMCs play an important role in reduction of restenosis rate. Combined treatment with ARB and statin after stenting is useful for preventing stent restenosis.

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Section: Introductionmentioning

confidence: 97%

Effects of Combined Treatment with Angiotensin II Type 1 Receptor Blocker and Statin on Stent Restenosis

Yasukawa

Nakamura²,

Nagase

et al. 2009

Journal of Cardiovascular Pharmacology

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“…The mevalonate isoprenoid biosynthesis pathway provides the cell with critical metabolic intermediates that are involved in multiple cellular processes . Inhibition of enzymes in this pathway with statins and bisphosphonates is clinically used in the respective treatment of hypercholesterolemia and metabolic bone disease . Farnesyl diphosphate (FPP) and geranylgeranyl diphosphate (GGPP) are two important isoprenoid intermediates at branch points of this pathway.…”

Section: Introductionmentioning

confidence: 99%

“…1,2 Inhibition of enzymes in this pathway with statins and bisphosphonates is clinically used in the respective treatment of hypercholesterolemia and metabolic bone disease. [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21] Farnesyl diphosphate (FPP) and geranylgeranyl diphosphate (GGPP) are two important isoprenoid intermediates at branch points of this pathway. Both FPP and GGPP serve as prenyl donors for protein isoprenylation, which is essential for many biological functions such as cell growth and cell proliferation.…”

Section: Introductionmentioning

confidence: 99%

Syntheses of deuterium labeled prenyldiphosphate and prenylcysteine analogues for in vivo mass spectrometric quantification

Subramanian

Sunkara

et al. 2013

Labelled Comp Radiopharmac

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A Wittig reaction employing Li(CD3)2CP(C6H5)3 was used to prepare d6-farnesol and d6-geranylgeraniol. Reductive amination of aniline-2,3,4,5,6-d5 was used to prepare the unnatural isoprenoid analogues d5-anilinogeraniol and d5-anilinofarnesol. All of these deuterated isoprenols were elaborated into their diphosphate and cysteine thioether derivatives suitable for use as stable-isotope labeled standards for quantitative mass spectrometric analysis.

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“…Statins also increase the activity of LDL receptors on cell membrane, accelerating the metabolism of very low-density lipoproteins (VLDL) remnant and LDL [16,17]. Even though drugs with such mechanism have an advantage to lower blood cholesterol level remarkably, but they exert serious adverse effects like hepatomegaly and renal hypertrophy [18,19].…”

mentioning

confidence: 99%

An ethanolic extract ofAngelica gigasimproves atherosclerosis by inhibiting vascular smooth muscle cell proliferation

et al. 2014

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The effects of an ethanolic extract of Angelica gigas (EAG) on the vascular smooth muscle cell (VSMC) proliferation and high-cholesterol diet-induced hypercholesterolemia and atherosclerosis were investigated. Rat aortic VSMCs were stimulated with platelet-derived growth factor-BB (25 ng/mL) for the induction of DNA synthesis and cell proliferation. EAG (1-10 µg/mL) significantly inhibited both the thymidine incorporation and cell proliferation in a concentration-dependent manner. Hypercholesterolemia was induced by feeding male New Zealand white rabbits with 0.5% cholesterol in diet for 10 weeks, during which EAG (1% in diet) was given for the final 8 weeks after 2-week induction of hypercholesterolemia. Hypercholesterolemic rabbits exhibited great increases in serum total cholesterol and low-density lipoproteins (LDL) levels, and finally severe atheromatous plaque formation covering 28.4% of the arterial walls. EAG significantly increased high-density lipoproteins (HDL), slightly decreased LDL, and potentially reduced the atheroma area to 16.6%. The results indicate that EAG attenuates atherosclerosis not only by inhibiting VASC proliferation, but also by increasing blood HDL levels. Therefore, it is suggested that EAG could be an alternative or an adjunct therapy for the improvement of hypercholesterolemia and atherosclerosis.

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3-Hydroxy-3-methylglutaryl coenzyme a (HMG-CoA) reductase inhibitors (statins), atherosclerosis and coronary syndromes

Cited by 13 publications

References 17 publications

Effects of Combined Treatment with Angiotensin II Type 1 Receptor Blocker and Statin on Stent Restenosis

Effects of Combined Treatment with Angiotensin II Type 1 Receptor Blocker and Statin on Stent Restenosis

Syntheses of deuterium labeled prenyldiphosphate and prenylcysteine analogues for in vivo mass spectrometric quantification

An ethanolic extract ofAngelica gigasimproves atherosclerosis by inhibiting vascular smooth muscle cell proliferation

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