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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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Regulation of urocortin I and its related peptide urocortin II by inflammatory and oxidative stresses in HL-1 cardiomyocytes.

TL;DR: The Ucn-CRH receptor system may be regulated by two major forms of cardiac stresses, i.e. oxidative and inflammatory stress, and may play a critical role in cardiac stress adaptation in heart diseases.
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Expressional patterns of cytokines in a murine model of acute myocarditis: early expression of cardiotrophin-1.

TL;DR: CT-1 expression preceded TNF-α and IL-1α expressions and active DNA synthesis in a murine model of acute myocarditis and may exert a protective role by modulating cytokine production and by inducing cardiomyocytic proliferation in CVB3-infected murine hearts.
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Beneficial effects of olmesartan, an angiotensin II receptor type 1 antagonist, in rats with dilated cardiomyopathy

TL;DR: It is demonstrated that olmesartan treatment significantly improved LV function and ameliorated the progression of cardiac remodeling in rats with DCM after EAM, a rat model in which myosin-induced experimental autoimmune myocarditis might develop into DCM.
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Anti-inflammatory therapy for heart failure

TL;DR: Accumulating evidence shows that heart failure is an inflammatory disease, and anti-inflammatory therapy by various agents would be a promising future treatment for heart failure.
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Clinical and neurohormonal correlates of circulating granulocyte-macrophage colony-stimulating factor in severe heart failure secondary to ischemic or idiopathic dilated cardiomyopathy

TL;DR: It is shown for the first time that granulocyte-macrophage colony-stimulating factor plasma levels are elevated in patients with severe heart failure, and these levels are correlated well with neurohormonal activation and hemodynamic deterioration characterizing this syndrome.
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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