The role of inflammatory cytokines in endothelial dysfunction

Zhang, Cuihua

doi:10.1007/s00395-008-0733-0

Cited by 396 publications

(311 citation statements)

References 74 publications

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“…This study included multiple biomarkers of inflammation and endothelial dysfunction, including CRP, sICAM-1, sE-selectin and angiotensin II; of the four, CRP, sICAM-1 and sE-selectin reflect the status of inflammation or the status of endothelial dysfunction. [25][26][27] In addition to its role as a vasoconstrictor, angiotensin II induces endothelial dysfunction and inflammation, resulting in accelerated progression of atherosclerosis. 28,29 Our study found that IR was related to the biomarkers of inflammation and endothelial dysfunction, both in subjects with hypertension and those without hypertension.…”

Section: Discussionmentioning

confidence: 99%

Co-effect of insulin resistance and biomarkers of inflammation and endothelial dysfunction on hypertension

Zhu

Wang

et al. 2012

Hypertens Res

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To explore the co-effects of inflammation and endothelial dysfunction and insulin resistance (IR) on hypertension in a large Asian population. Data on demographic characteristics, blood pressure and other variables were collected; additionally, fasting plasma glucose, insulin and biomarkers, including C-reactive protein (CRP), soluble intercellular cell adhesion molecule-1 (sICAM-1), soluble E-selectin (sE-selectin) and angiotensin II were examined among 2553 Mongolian adults aged X20 years. IR was assessed using the homeostasis model. The co-effects of elevated biomarkers of inflammation and endothelial dysfunction and IR on hypertension were analyzed. A total of 953 subjects were diagnosed with hypertension. Among hypertensive subjects, the levels of CRP (11.0 vs. 6.7 mg l À1 ), sICAM-1 (348.3 vs. 335.9 ng ml À1 ), sE-selectin (20.9 vs. 18.5 ng ml À1 ) and angiotensin II (61.3 vs. 50.0 pg ml À1 ) were significantly higher among subjects with IR than those without IR; among normotensives, levels of CRP (6.3 vs. 5.2 mg l À1 ) and sE-selectin (20.1 vs. 17.8 ng ml À1 ) were higher among IR subjects than those without IR. The prevalence of hypertension was significantly higher among subjects with IR and 2 elevated biomarkers (69.0%) and those with IR and X3 elevated biomarkers (79.3%) than among those with IR and no elevated biomarkers (45.9%) and those with IR and 1 elevated biomarker (50.6%). After adjusting for multivariate, the risk of hypertension was significantly associated with the coexistence of IR and any two or three elevated biomarkers (odds ratios (OR) (95% confidence intervals (CIs))¼2.55 (1.60-4.06) and 3.19 (1.15-8.86), respectively). In this Mongolian population, IR and elevated biomarkers of inflammation and endothelial dysfunction were related to hypertension and the coexistence of IR and elevated biomarkers of inflammation and endothelial dysfunction increased the risk of hypertension.

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Section: Discussionmentioning

confidence: 99%

Co-effect of insulin resistance and biomarkers of inflammation and endothelial dysfunction on hypertension

Zhu

Wang

et al. 2012

Hypertens Res

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“…Several investigators clearly demonstrated that inflammatory mediators induced endothelial dysfunction. 43 Qamirani et al 44 reported that CRP inhibits endothelium-dependent NOmediated dilation in coronary arterioles by producing superoxide from NAD(P)H oxidase through p38 kinase activation. The present study demonstrated that olmesartan significantly reduced serum hsCRP levels as previously reported.…”

Section: Discussionmentioning

confidence: 99%

Olmesartan improves endothelial function in hypertensive patients: link with extracellular superoxide dismutase

et al. 2011

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Endothelial dysfunction in essential hypertension is an independent predictor for future cardiovascular events. Although inhibition of the renin-angiotensin system (RAS) reportedly improves endothelial function through its effects on oxidative stress and inflammation, questions remain regarding the factors that are pivotal for improvement of endothelial function by RAS inhibition. We therefore performed a prospective, randomized crossover trial in which an angiotensin II type 1 receptor antagonist, olmesartan and calcium channel blocker, amlodipine, were compared in 31 essential hypertensive patients. Results showed that, although both treatments achieved comparable lowering of blood pressure (BP), olmesartan, but not amlodipine, significantly improved endothelial function as evaluated by flow-mediated vasodilation (FMD) in the brachial artery. Although no significant changes in diabetic and lipid parameters were observed with either drug, olmesartan slightly decreased estimated glomerular filtration rate, which, surprisingly, translated into decreased microalbuminuria. In a similar vein, olmesartan reduced serum C-reactive protein and increased urine antioxidant levels compared with baseline, and reduced urine 8-epi-prostaglandin F2a levels compared with both baseline and amlodipine. Finally, although overall changes in plasma extracellular superoxide dismutase (EC-SOD) levels were not modulated by either treatment, for olmesartan there was a positive correlation between changes in FMD and those in EC-SOD levels. In conclusion, olmesartan improved endothelial function in hypertensive patients independent of its BP-lowering effect, which was due, at least in part, to its antioxidative property. Therefore, olmesartan might provide a greater long-term benefit for hypertensive patients with impaired endothelial function than amlodipine.

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“…AS is a commonly recognized inflammatory disease [2][3][4] , although the mechanism of its initiation and progression is not fully understood.…”

Section: Introductionmentioning

confidence: 99%

Angiogenesis Inhibitor, Endostar, Prevents Vasa Vasorum Neovascularization in a Swine Atherosclerosis Model

Xu¹,

Mao²,

Chai

et al. 2015

J Atheroscler Thromb

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Aim:Vasa vasorum neovascularization is a key feature of atherosclerosis (AS) and is strongly associated with inflammatory infiltration, lipid deposition, intraplaque hemorrhage, and hemosiderin deposit. Here we investigate the effects of Endostar, a strong anti-angiogenic drug, on vasa vasorum neovascularization in the experimental porcine model of early AS. Methods: Eighteen adult male Ba-Ma mini pigs were randomized into three groups, with six animals in each group. The pigs in the normal (N) group were fed a normal diet for 18 weeks, without balloon injury surgery. The animals in the atherosclerotic (AS) control and AS Endostar groups were fed a hypercholesterolemic diet for 12 weeks after balloon injury surgery; they received either saline or Endostar for an additional six weeks, while continuing the hypercholesterolemic diet. The atherosclerotic abdominal aorta and levels of serum lipids, TNF-alpha, IL-6, and hs-CRP were analyzed at 18 weeks. Results: The AS group had a significantly higher body weight and serum lipid concentration levels than the N group (p 0.05), confirming the success of the hypercholesterolemic diet. However, no statistical differences were noted between the AS and AS Endostar groups. Histopathology results revealed that vasa vasorum density and intima -media thickness (IMT) had also increased in the AS group compared with those in the N group (p 0.05). The Endostar treatment significantly alleviated AS with decreased vasa vasorum density and IMT (AS vs. AS Endostar, p 0.05). Western blot analysis indicated that the expression of VEGF, -catenin, and TNF-alpha in the atherosclerotic abdominal aorta was considerably reduced by the Endostar treatment. In addition, immunohistochemistry results showed that the angiogenesis markers VEGF and -catenin were predominately localized in endothelial cells of the adventitial vasa vasorum. The levels of the serum inflammatory markers TNF-alpha, hs-CRP, and IL-6 were markedly higher in the AS group than in the N group (p 0.05) but showed no marked difference during the Endostar treatment, suggesting that the local inhibition of angiogenesis was not accompanied by a change in serum inflammatory markers and that the inhibitive effect of Endostar on local TNF-alpha expression could be because of the prevention of vasa vasorum neovascularization. Conclusions: Our results demonstrated that the Endostar treatment inhibited vasa vasorum neovascularization and AS progression in the experimental porcine model of early AS, supporting the role of vasa vasorum neovascularization in the development of AS and the therapeutic potential of antiangiogenesis intervention in AS.

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The role of inflammatory cytokines in endothelial dysfunction

Cited by 396 publications

References 74 publications

Co-effect of insulin resistance and biomarkers of inflammation and endothelial dysfunction on hypertension

Co-effect of insulin resistance and biomarkers of inflammation and endothelial dysfunction on hypertension

Olmesartan improves endothelial function in hypertensive patients: link with extracellular superoxide dismutase

Angiogenesis Inhibitor, Endostar, Prevents Vasa Vasorum Neovascularization in a Swine Atherosclerosis Model

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