The effect of fluvastatin on catheter-induced intimal thickening in normocholesterolemic rabbits

Ye, P; Yu, Dongliang; Song, Liqiang

doi:10.1016/s0021-9150(00)80158-6

Cited by 4 publications

(11 citation statements)

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“…These results were subsequently reproduced by other workers using fluvastatin (8 mg/kg/day, po) [46] or simvastatin (2 or 20 mg/kg/day, sc) [49] in various models of catheter-induced vascular injury. More recently, Nishimura et al reported similar findings with simvastatin (2 mg/kg/day, po) in a rat model of chemically induced pulmonary artery hypertension [44].…”

Section: From Bench To Body: Clinical Relevance Of Statininduced Apopsupporting

confidence: 63%

“…H-ras suppression and p53 induction have also been documented upon in vivo statin treatment [46], where downstream effectors of the classical MAPK (c-fos) and p38 / JNK (c-jun) signalling pathways are also downregulated [44]. Taken together these observations suggest that statins may also directly intercept growth factor receptor signalling, probably at the level of Ras (Fig.…”

Section: Statins and The Cell Cyclementioning

confidence: 72%

“…More recently, Nishimura et al reported similar findings with simvastatin (2 mg/kg/day, po) in a rat model of chemically induced pulmonary artery hypertension [44]. It is intriguing that statin treatment preferentially augmented apoptosis in manipulated / injured arteries but not in intact vascular tissue [39,46,49]. Since active cellular proliferation and differentiation only occurs in the former setting, these findings may be taken to illustrate the importance of predisposing factors for in vivo manifestation of statininduced apoptosis.…”

Section: From Bench To Body: Clinical Relevance Of Statininduced Apopmentioning

confidence: 76%

“…Since active cellular proliferation and differentiation only occurs in the former setting, these findings may be taken to illustrate the importance of predisposing factors for in vivo manifestation of statininduced apoptosis. Furthermore, while none of these reports provided information on systemic drug levels, statin treatment at the aforementioned doses did not affect blood lipid levels [39,46,49], implying that significant in vivo statin-induced apoptosis may indeed occur on clinically suboptimal drug exposure.…”

Section: From Bench To Body: Clinical Relevance Of Statininduced Apopmentioning

confidence: 98%

“…Further reported changes in the molecular machinery of the cell cycle upon in vitro exposure to statins include downregulation of H-ras [17,46], p38 and MAPK activity [47,48], PCNA [46,48] and cyclin A [23]; conversely, p53 [32,42,46] and mitosin (a centromere-associated protein) [27] are induced. H-ras suppression and p53 induction have also been documented upon in vivo statin treatment [46], where downstream effectors of the classical MAPK (c-fos) and p38 / JNK (c-jun) signalling pathways are also downregulated [44].…”

Section: Statins and The Cell Cyclementioning

confidence: 99%

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Threes Company: Regulation of Cell Fate by Statins

Vamvakopoulos¹

2005

CDTCHD

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Inhibitors of 3-hydroxy-3-methylglutaryl-CoA reductase (statins), the rate-limiting enzyme of the mevalonate biosynthetic pathway, are currently the leading prescription drugs worldwide. Programmed cell death (apoptosis) is a powerful physiological regulator of cellular development, function and dynamics. Statins are known to induce cellular apoptosis in vitro; however, the clinical relevance of this action remains controversial. This paper draws from 15 years' worth of research to explore the impact of statin treatment on cell fate, as represented by the interlinked processes of cellular growth, differentiation and apoptosis. In particular, I outline our current understanding of the pertinent molecular mechanisms; and discuss the evidence for clinical relevance of statin-induced apoptosis.

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Section: From Bench To Body: Clinical Relevance Of Statininduced Apopsupporting

confidence: 63%

Section: Statins and The Cell Cyclementioning

confidence: 72%

Section: From Bench To Body: Clinical Relevance Of Statininduced Apopmentioning

confidence: 76%

Section: From Bench To Body: Clinical Relevance Of Statininduced Apopmentioning

confidence: 98%

Section: Statins and The Cell Cyclementioning

confidence: 99%

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Threes Company: Regulation of Cell Fate by Statins

Vamvakopoulos¹

2005

CDTCHD

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Cholesterol-lowering strategies reduce vascular LRP1 overexpression induced by hypercholesterolaemia

Llorente‐Cortés¹,

Casaní²,

Cal³

et al. 2011

European Journal of Clinical Investigation

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Chronic treatment with pravastatin prevents early cardiovascular changes in spontaneously hypertensive rats

Kassan

Montero

Sevilla

2009

British J Pharmacology

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Background and purpose:This study investigates the effect of pravastatin on blood pressure, cardiovascular remodelling and impaired endothelial function induced as early signs of cardiovascular disease in young spontaneously hypertensive rats (SHR). Experimental approach: Eight-week-old SHR were treated for 4 weeks with pravastatin (20 mg·kg). Systolic blood pressure was measured periodically during the study using the tail-cuff method. At the end of the study, the left ventricular weight /body weight ratio was used as an index of left ventricular hypertrophy (LVH). Vascular function, superoxide (O2 -.) production and structure were studied in aortic rings. Lipid peroxidation was measured in plasma (thiobarbituric acid reactive substances assay). Key results: Systolic blood pressure was lower in treated SHR than in control SHR, at the end of the study (171 Ϯ 1 vs. 159 Ϯ 2 mmHg, P < 0.05), and LVH was significantly reduced by pravastatin (2.7 Ϯ 0.02 vs. 2.5 Ϯ 0.01 mg·g -1 , P < 0.05). Vascular responses to sodium nitroprusside and phenylephrine were similar in both groups; nevertheless, the relaxation response to acetylcholine was higher in the treated rats (45.6 Ϯ 2.6 vs. 58.1 Ϯ 3.2 %, P < 0.05). Vascular O2 -. and plasma thiobarbituric acid reactive substances were reduced by pravastatin treatment, and urinary nitrites was elevated. Finally aortic wall became thinner after pravastatin treatment. Conclusions and implications: Chronic treatment with pravastatin attenuated the increase of systolic blood pressure in SHR, prevented early LVH and improved vascular structure and function. These effects were accompanied by decreased measures of oxidative stress and improvements in NO production.

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The effect of fluvastatin on catheter-induced intimal thickening in normocholesterolemic rabbits

Cited by 4 publications

References 0 publications

Threes Company: Regulation of Cell Fate by Statins

Threes Company: Regulation of Cell Fate by Statins

Cholesterol-lowering strategies reduce vascular LRP1 overexpression induced by hypercholesterolaemia

Chronic treatment with pravastatin prevents early cardiovascular changes in spontaneously hypertensive rats

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