Circulating Levels of Cytokines and Their Endogenous Modulators in Patients With Mild to Severe Congestive Heart Failure Due to Coronary Artery Disease or Hypertension

Testa, Marco; Yeh, Michael; Lee, Paul; Berman, Joan W.; LeJemtel, Thierry H.; Fanelli, Raffaele; Loperfido, Francesco

doi:10.1016/s0735-1097(96)00268-9

Cited by 469 publications

(314 citation statements)

References 21 publications

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“…We also observed that Ang (1-7) treatment reduced the elevated levels of IL-1b, IL-6 and TNF-a expression in the failing myocardium. Several studies have shown that in both animals and humans with failing hearts, levels of inflammatory cytokines (e.g., IL-1b, IL-6 and TNF-a) are increased in the plasma 20,21 and in the circulating leukocytes, 22 as well as in the myocardium itself. [23][24][25] Our observation that the levels of IL-1b, IL-6 and TNF-a were elevated in the failing myocardium of mice, 12 weeks after 5/6 NC, is consistent with those of earlier findings.…”

Section: Angiotensin (1à7) Prevent Heart Dysfunction and Left Ventricmentioning

confidence: 99%

Angiotensin (1−7) prevent heart dysfunction and left ventricular remodeling caused by renal dysfunction in 5/6 nephrectomy mice

et al. 2009

Hypertens Res

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The renin-angiotensin system (RAS) plays a critical role in chronic renal failure associated with heart failure. In the past few years, angiotensin (Ang) (1-7) have been reported to counteract the effects of angiotensin II (Ang II) and were even considered as a new therapeutical target in RAS. The purposes of this study were to examine whether the Ang (1-7) improves the heart function and remodeling of the left ventricle (LV) in mice with 5/6 nephrectomy (NC). We used a 5/6 nephrectomy to induce significant renal dysfunction in wildtype mice (WT). Twelve weeks after NC, WT showed high blood pressure, significant leftventricular dilation and dysfunction, which were accompanied by cardiomyocyte hypertrophy, diffuse interstitial fibrosis and oxidative damage of cardiomyocytes. Exogenous Ang (1-7) injection improved the heart function and remodeling of LV in mice with 5/6 NC accompanied by a reduction in cardiac interstitial fibrosis, inflammatory cytokine expression and oxidative damage levels of cardiomyocytes, decrease in the profibrotic signaling molecule transforming growth factor (TGF)-b and increase in the collagen degradation signaling molecule matrix metalloproteinase (MMP)-2, -9. However, these beneficial effects did not occur in hydralazine-treated mice. These findings suggest that (1) Exogenous Ang (1-7) injection improve the heart function and remodeling of LV in mice with 5/6 NC. (2) These beneficial effects are independent of its anti-blood pressure effect.

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Section: Angiotensin (1à7) Prevent Heart Dysfunction and Left Ventricmentioning

confidence: 99%

Angiotensin (1−7) prevent heart dysfunction and left ventricular remodeling caused by renal dysfunction in 5/6 nephrectomy mice

et al. 2009

Hypertens Res

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“…Plasma levels of angiotensin II, tumour necrosis factor-α (TNF-α), and interleukin-1β increase as symptoms worsen in patients with advanced HF [24]. Cytokines activate NAD(P)H oxidase, thereby increasing superoxide production [25][26][27].…”

Section: "Systemic Endothelitis" In Acute Heart Failurementioning

confidence: 99%

Acute heart failure as “acute endothelitis” — Interaction of fluid overload and endothelial dysfunction

Colombo

Onat

Sabbah

2008

European J of Heart Fail

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“…The aforementioned cytokines play a dual role, activating apoptosis in myocytes (13), while also functioning in a cytoprotective manner (15). Furthermore, inappropriate activation of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) have been recognized as an important mediator in the development of endothelial dysfunction, cardiac hypertrophy, and heart failure in experimental animal models and in humans (9,17,28,30). Atrial natriuretic peptide (ANP) has been shown to inhibit the TNF-α induced adhesion molecule expression in endothelial cells (32).…”

Section: Introductionmentioning

confidence: 99%

Enhanced activation of pro-inflammatory cytokines in mice lacking natriuretic peptide receptor-A

2007

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Natriuretic peptide receptor-A (NPRA) is the principal receptor for the cardiac hormones ANP and BNP. Mice lacking NPRA develop progressive cardiac hypertrophy and congestive heart failure. However, the mechanisms responsible for hypertrophic growth in the absence of NPRA signaling are not yet known. In the present study, we determined whether deficiency of NPRA/cGMP signaling alters the cardiac pro-inflammatory cytokines gene expression in Npr1 (coding for NPRA) geneknockout (Npr1 −/− ) mice exhibiting cardiac hypertrophy and fibrosis as compared with control wildtype (Npr1 +/+ ) mice. A significant up-regulation of cytokine genes such as TNF-α (5-fold), IL-6 (3-fold) and TGF-β1 (4-fold) were observed in mutant mice hearts lacking NPRA as compared with the age-matched wild-type mice. In parallel, NF-κB binding activity was almost 5-fold greater in the nuclear extract of Npr1 −/− mutant mice hearts as compared with wild-type Npr1 +/+ mice hearts. Guanylyl cyclase (GC) activity and cGMP levels were drastically reduced by 10-fold and 6-fold, respectively, in ventricular tissues of mutant mice hearts relative to wild-type controls. The present findings provide direct evidence that ablation of NPRA/cGMP signaling activates inflammatory cytokines, probably via NF-κB mediated signaling pathway, and is associated with hypertrophic growth of null mutant mice hearts.

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Circulating Levels of Cytokines and Their Endogenous Modulators in Patients With Mild to Severe Congestive Heart Failure Due to Coronary Artery Disease or Hypertension

Cited by 469 publications

References 21 publications

Angiotensin (1−7) prevent heart dysfunction and left ventricular remodeling caused by renal dysfunction in 5/6 nephrectomy mice

Angiotensin (1−7) prevent heart dysfunction and left ventricular remodeling caused by renal dysfunction in 5/6 nephrectomy mice

Acute heart failure as “acute endothelitis” — Interaction of fluid overload and endothelial dysfunction

Enhanced activation of pro-inflammatory cytokines in mice lacking natriuretic peptide receptor-A

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