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Increased circulating cytokines inpatients with myocarditis andcardiomyopathy

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TLDR
In this paper, the potential role of cytokines in the pathogenesis of cardiomyopathy and myocarditis was elucidated, and experimental studies showed that certain cytokines depress myocardial
Abstract
Objectives-To elucidate thepotential roleofcytokines inthepathogenesis of cardiomyopathy andmyocarditis. Background-Experimental studies show thatcertain cytokines depress myocardial

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Persistent Expression of Cytokines inÈthe Chronic Stage of CVB3-induced Myocarditis in NMRI Mice

TL;DR: Data indicate that the persistence of viral RNA is associated with persistently high levels of cytokine mRNAs which, when translated, could severely contribute to pathological changes and injury of connective tissue in the chronic stage of myocarditis.
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TNF-α increases cardiac fibroblast lysyl oxidase expression through TGF-β and PI3Kinase signaling pathways.

TL;DR: The results indicate that TNF-α stimulated LOX expression may play an important role in progressive cardiac fibrosis, and inhibition of TGF-β receptor I or Smad3 prevented increased LOXexpression by TNFs.
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Cytokines and their receptors in cardiovascular diseases--role of gp130 signalling pathway in cardiac myocyte growth and maintenance.

TL;DR: Activation of gp130 transduces hypertrophic and cytoprotective signals in cardiac myocytes via JAK/STAT, MAP kinase and PI‐3 kinase pathways may be a newly discovered mechanism that regulates these events in association with cy toprotective effect in myocardial diseases.
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Adenosine and cardioprotection in the diseased heart.

TL;DR: In this article, the authors found that ecto-5'-nucleotidase activation activated the enzyme responsible for adenosine release, which may act as an endogenous cardioprotective substance in pathophysiological conditions of the heart.
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Tumor necrosis factor-alpha promoter polymorphisms in Mexican patients with rheumatic heart disease

TL;DR: The data demonstrate that RHD is associated with TNF-alpha polymorphisms in the Mexican population; however, these polymorphisms do not have relation with the valve damage.
References
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Elevated Circulating Levels of Tumor Necrosis Factor in Severe Chronic Heart Failure

TL;DR: It is indicated that circulating levels of tumor necrosis factor are increased in cachectic patients with chronic heart failure and that this elevation is associated with the marked activation of the renin-angiotensin system seen in patients with end-stage cardiac disease.
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Negative inotropic effects of cytokines on the heart mediated by nitric oxide

TL;DR: The findings demonstrate that the direct negative inotropic effect of cytokines is mediated through a myocardial nitric oxide synthase, and the regulation of pro-inflammatory cytokines and myocardia nitricoxide synthase may provide new therapeutic strategies for the treatment of cardiac disease.
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A molecular basis for familial hypertrophic cardiomyopathy: A β cardiac myosin heavy chain gene missense mutation

TL;DR: Identification of two unique mutations within cardiac MHC genes in all individuals with FHC from two unrelated families demonstrates that defects in the cardiac M HC genes can cause this disease.
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Characteristics and Prognostic Implications of Myosin Missense Mutations in Familial Hypertrophic Cardiomyopathy

TL;DR: It is suggested that the precise definition of the disease-causing mutation can provide important prognostic information about affected members in families with hypertrophic cardiomyopathy.
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