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• W201853504 abstract "Congestive heart failure (CHF) may be produced by a variety of disorders, including dilated cardiomyopathy, hypertensive heart disease, and ischemic heart disease. We have developed experimental models of these diseases. In a murine model of myocarditis, inflammatory cytokines were induced rapidly in the myocardium, and remained expressed during the chronic stage, when the heart had developed the typical characteristics of dilated cardiomyopathy. In the pressure-overloaded ventricle, the myocardium developed adaptive hypertrophy before its transition to heart failure, a process in which cytokines appeared to play a significant role by accelerating myocyte growth and down-modulating cardiac function. In the ischemic heart, the non-ischemic myocardium developed hypertrophy associated with progression of scarring in the ischemic area. This remodeling process initially represents an important compensatory mechanism to preserve ventricular function, though later leads to the development of heart failure. During this phase of healing from acute ischemia, inflammatory cytokines were persistently upregulated in the non-ischemic myocardium. Thus, we hypothesized that some aspects of heart failure may be mediated by reversible alterations of cardiac function and structural changes in the ventricle induced by cytokines. In the respect, several drugs used routinely in clinical practice have been proved to modulate the production of cytokines, suggesting that immunomodulating or anticytokine therapy may represent a new approach to the management of heart failure [1]." @default.
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• W201853504 date "2001-01-01" @default.
• W201853504 modified "2023-10-16" @default.
• W201853504 title "Immunomodulation of Cytokines in Experimental Models of Heart Failure" @default.
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• W201853504 doi "https://doi.org/10.1007/978-1-4615-1449-7_8" @default.
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