Regular ArticleInducible Nitric Oxide Synthase (iNOS) in the Human Heart: Expression and Localization in Congestive Heart Failure☆
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Redox signaling in heart failure and therapeutic implications
2021, Free Radical Biology and MedicineCitation Excerpt :Expression of iNOS is low in the heart, but induced by different stimuli such as inflammatory mediators (e.g., cytokines) or hypoxia [180,181]. After induction, iNOS produces large amounts of NO, accompanied by OONO− and O2•− production [180,182], contributing to contractile dysfunction in HF [183]. In cardiomyocytes, nNOS localizes primarily in the SR [184], but was also detected in the sarcolemmal membrane [185], mitochondria [186] and the Golgi apparatus [187,188].
TRPV<inf>1</inf> channels in cardiovascular system: A double edged sword?
2017, International Journal of CardiologyCitation Excerpt :Activation of PPAR-δ [43] and UCP2 [30] play an important role in reducing oxidative stress-induced apoptosis in the cells. Moreover, iNOS, which is not usually expressed in the healthy heart, is enhanced in response to stimuli including tissue injury and inflammation [59]. Reduction in iNOS expression in myocardium can inhibit the initiation of events that lead to cardiac remodeling [23].
Testosterone and resistance training effects on muscle nitric oxide synthase isoforms in COPD men
2012, Respiratory MedicineCitation Excerpt :Montes-de-Oca et al. reported decreased eNOS and nNOS levels, as well as markedly elevated iNOS levels in muscles of severe COPD patients.16 These high iNOS isoform levels might lead to toxic amounts of NO and contribute to muscle dysfunction in COPD as well as in other chronic diseases such as congestive heart failure.19–22 It has been shown that exercise training in chronic heart failure patients modifies the NOS system.23
Inflammation in Heart Failure—Future Perspectives
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2021, Frontiers in Physiology
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Please address all correspondence to: Niels G. Vejlstrup, Dept of Medicine B 2142, Rigshospitalet, Blegdamsvej 9, 2100 Copenhagen, Denmark.