Key result
Increased expression of inducible nitric oxide synthase (iNOS) in the myocardium, driven by cytokines and neurohumoral factors, may cause cardiac dysfunction and cell damage in chronic heart failure.
Increased iNOS expression induced by cytokines and neurohumoral factors in chronic heart failure may contribute to cardiac dysfunction and myocyte damage.
May link cytokine-driven iNOS to HF progression; leaves open whether selective inhibition alters outcomes in dilated cardiomyopathy.
Cardiac myocytes express two types of nitric oxide (NO) synthase, eNOS and iNOS. eNOS activity is regulated by the contractile state of the heart, while iNOS expression is induced by cytokines. Nitric oxide induced by cytokines causes negative inotropic and lethal effects on cardiac myocytes. Expression of iNOS in the myocardium is increased in patients with dilated cardiomyopathy with clinical evidence of heart failure. Several neurohumoral factors activated in chronic heart failure augment cardiac iNOS expression and could cause cardiac dysfunction and cell damage.
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Ikeda et al. (1997) conducted a review in Heart failure and dilated cardiomyopathy. Nitric oxide / iNOS expression was evaluated. Increased expression of inducible nitric oxide synthase (iNOS) in the myocardium, driven by cytokines and neurohumoral factors, may cause cardiac dysfunction and cell damage in chronic heart failure.
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