Molecular and immune mechanisms in the pathogenesis of cardiomyopathy--role of viruses, cytokines, and nitric oxide.
Myocarditis is thought to be commonly caused by various viruses, and accumulating evidence links viral myocarditis with the eventual development of dilated cardiomyopathy. Recently, the importance of hepatitis C virus infection was noted in patients with dilated and hypertrophic cardiomyopathy. Cytokines are being increasingly recognized as an important factor in the pathogenesis and pathophysiology of myocarditis and cardiomyopathy. Elevated levels of circulating cytokines have been reported in patients with heart failure, and various cytokines have been shown to depress myocardial contractility in vitro and in vivo. A number of reports have shown that cytokines generated by activated immune cells cause an increase in nitric oxide (NO) via induction of NO synthase. Increased generation of NO may induce negative inotropism and myocardial damage. This review discusses the etiology and pathogenesis of myocarditis and cardiomyopathy from this point of view.
Matsumori
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Department of Cardiovascular Medicine, Kyoto University, Japan.
D000818:Animals; D009202:Cardiomyopathies / Q000276:immunology / Q000378:metabolism / Q000821:virology; D002311:Cardiomyopathy, Dilated / Q000276:immunology / Q000378:metabolism / Q000821:virology; D002312:Cardiomyopathy, Hypertrophic / Q000276:immunology / Q000378:metabolism / Q000821:virology; D016207:Cytokines / Q000502:physiology*; D006526:Hepatitis C / Q000150:complications*; D006801:Humans; D009205:Myocarditis / Q000276:immunology / Q000378:metabolism / Q000821:virology; D009569:Nitric Oxide / Q000096:biosynthesis*
D016207:Cytokines; D009569:Nitric Oxide