Statins to prevent cardiovascular events in hypertensive patients. The ASCOT-LLA study

Osende, Julio I.; Ruíz-Ortega, Marta; Blanco-Colio, Luís Miguel; Egido, Jesús

doi:10.1093/ndt/gfg538

Cited by 13 publications

(6 citation statements)

References 19 publications

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“…A potential explanation is the effect on pro-inflammatory parameters, as discussed in the present review. Moreover, combination of RAS blockers with other drugs, such as statins, that present anti-inflammatory properties exerts additive beneficial effects, due to their modulation of cell responses, including activation of the Rho pathway [94]. The data reviewed here provide a rationale for the use of RAS blockers alone or in combination to prevent vascular and renal inflammatory response in patients with hypertension.…”

Section: Resultsmentioning

confidence: 96%

Renal and vascular hypertension-induced inflammation: role of angiotensin II

Ruíz-Ortega

Esteban

Rupérez

et al. 2006

Current Opinion in Nephrology and Hypertension

136

107

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The pharmacological blockade of angiotensin II actions, by angiotensin-converting enzyme inhibitors or angiotensin receptor antagonists, results in beneficial organ protective effects, in addition to the effects of these agents on blood pressure control, that can be explained by the blockade of the angiotensin II-induced pro-inflammatory response. These data provide a rationale for the use of blockers of the renin-angiotensin system to prevent vascular and renal inflammation in patients with hypertension.

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Section: Resultsmentioning

confidence: 96%

Renal and vascular hypertension-induced inflammation: role of angiotensin II

Ruíz-Ortega

Esteban

Rupérez

et al. 2006

Current Opinion in Nephrology and Hypertension

136

107

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“…These therapeutic interventions, in particular statin therapy, ACE inhibition, and arginine supplementation, have shown some improvements in these disease settings. Statins, which were initially designed as lipid-lowering drugs, demonstrate lipid-independent effects such as partially restoring EDNO levels and decreasing oxidative stress in hypertensive and hypercholesterolaemic patients [ 48 , 49 ]. These improvements occurred more rapidly than the decline in cholesterol levels [ 48 ], suggesting that one of the pleiotropic effects of statins is to enhance endothelial function by upregulating EDNO signaling.…”

Section: Improving Endothelial Function: a Clinical Perspectivementioning

confidence: 99%

Targeting Endothelial Dysfunction in Vascular Complications Associated with Diabetes

Sharma

Bernatchez

2012

International Journal of Vascular Medicine

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Cardiovascular complications associated with diabetes remain a significant health issue in westernized societies. Overwhelming evidence from clinical and laboratory investigations have demonstrated that these cardiovascular complications are initiated by a dysfunctional vascular endothelium. Indeed, endothelial dysfunction is one of the key events that occur during diabetes, leading to the acceleration of cardiovascular mortality and morbidity. In a diabetic milieu, endothelial dysfunction occurs as a result of attenuated production of endothelial derived nitric oxide (EDNO) and augmented levels of reactive oxygen species (ROS). Thus, in this review, we discuss novel therapeutic targets that either upregulate EDNO production or increase antioxidant enzyme capacity in an effort to limit oxidative stress and restore endothelial function. In particular, endogenous signaling molecules that positively modulate EDNO synthesis and mimetics of endogenous antioxidant enzymes will be highlighted. Consequently, manipulation of these unique targets, either alone or in combination, may represent a novel strategy to confer vascular protection, with the ultimate goal of improved outcomes for diabetes-associated vascular complications.

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“…Statins, as the first-line agents in hypercholesteremia therapy, have benefits in hypertensive patients and are able to lower the risk of developing cardiovascular events (18). Since hypertension is a common complication of traditional anti-angiogenic therapy in patients with cancer (19), the supply of statins is an attractive strategy in cancer treatment.…”

Section: Discussionmentioning

confidence: 99%

Expression profile of apoptotic and proliferative proteins in hypoxic HUVEC treated with statins

Li¹,

Liu²,

Xu³

et al. 2014

International Journal of Oncology

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Vascular endothelial hyperproliferation is involved in the pathophysiological process of angiogenesis, which is indispensable for tumor growth and spread in hypoxic adaptation. There is increasing evidence indicating that statins have potential anti-angiogenesis benefits. However, the intracellular signaling mechanism underlying the effect of statins in vascular endothelial cells is undefined. The present study was conducted to investigate the effect of fluvastatin on cell proliferation and apoptosis in normoxic and hypoxic human umbilical vein endothelial cells (HUVEC). Flow cytometric analyses revealed that statins reversed hypoxia-induced cell proliferation by slowing down G1 to S transition and inducing cell apoptosis. To get further insights into the downstream effects of statins, we measured the expression of various apoptosis-associated proteins in hypoxic HUVEC using human apoptosis antibody array. The results suggested that cell apoptosis was accompanied by upregulation of caspase-3, p27, IGFBP-6 and a decrease of bcl-2, survivin levels. Subsequent studies confirmed the results of array and demonstrated that fluvastatin activated mitochondrial apoptosis through enhancing bax/bcl-2 ratio, releasing cytochrome c, in turn activating caspase-9 and caspase-3, and eventually cleaving PARP. Further experiments showed that inhibition of cell proliferation by fluvastatin was associated with elevated IGFBP-6, p27, p53 levels and reduced survivin, cyclin B1, cyclin D1 and VEGF expression. Taken together, fluvastatin suppressed cell proliferation and induced apoptosis of HUVEC in hypoxia via multiple signaling pathways, providing a theoretical basis for statins in the therapy of cancer.

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Statins to prevent cardiovascular events in hypertensive patients. The ASCOT-LLA study

Cited by 13 publications

References 19 publications

Renal and vascular hypertension-induced inflammation: role of angiotensin II

Renal and vascular hypertension-induced inflammation: role of angiotensin II

Targeting Endothelial Dysfunction in Vascular Complications Associated with Diabetes

Expression profile of apoptotic and proliferative proteins in hypoxic HUVEC treated with statins

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