Expression of p22-phox and gp91-phox, Essential Components of NADPH Oxidase, Increases after Myocardial Infarction

Fukui, Toshiki; Yoshiyama, Minoru; Hanatani, Akihisa; Omura, Takashi; Yoshikawa, Junichi; Abe, Youichi

doi:10.1006/bbrc.2001.4493

Cited by 105 publications

(72 citation statements)

References 30 publications

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“…Similar NADPH oxidase activation is also observed in pressure-overload LVH in mice (Byrne et al 2003). An increased cardiac expression of the NADPH oxidase subunits, NOX2 and p22 phox , was also reported after myocardial infarction both in an animal model (Fukui et al 2001) and in human myocardium (Krijnen et al 2003). Recently, our group and others confirmed that myocardium from end-stage human CHF patients demonstrates increased NADPH oxidase activity (Heymes et al 2003;Maack et al 2003).…”

Section: Involvement Of Nadph Oxidases In Lvh and Heart Failuresupporting

confidence: 62%

NADPH oxidase-derived reactive oxygen species in cardiac pathophysiology

Cave

Grieve

Johar

et al. 2005

Phil. Trans. R. Soc. B

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Chronic heart failure, secondary to left ventricular hypertrophy or myocardial infarction, is a condition with increasing morbidity and mortality. Although the mechanisms underlying the development and progression of this condition remain a subject of intense interest, there is now growing evidence that redox-sensitive pathways play an important role. This article focuses on the involvement of reactive oxygen species derived from a family of superoxide-generating enzymes, termed NADPH oxidases (NOXs), in the pathophysiology of ventricular hypertrophy, the accompanying interstitial fibrosis and subsequent heart failure. In particular, the apparent ability of the different NADPH oxidase isoforms to define the response of a cell to a range of physiological and pathophysiological stimuli is reviewed. If confirmed, these data would suggest that independently targeting different members of the NOX family may hold the potential for therapeutic intervention in the treatment of cardiac disease.

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Section: Involvement Of Nadph Oxidases In Lvh and Heart Failuresupporting

confidence: 62%

NADPH oxidase-derived reactive oxygen species in cardiac pathophysiology

Cave

Grieve

Johar

et al. 2005

Phil. Trans. R. Soc. B

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“…Fukui et al [102] were one of the first groups to suggest the involvement of NADPH oxidases in post-MI remodeling. These authors observed elevated Nox2 and p22phox expression levels in the rat myocardium after experimental MI.…”

Section: Ventricular Remodeling After Myocardial Infarctionmentioning

confidence: 99%

NADPH oxidase signaling and cardiac myocyte function

Akki

Zhang

Murdoch

et al. 2009

Journal of Molecular and Cellular Cardiology

124

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“…Multiple factors may, in fact, contribute to left ventricular remodeling at different stages postMI. There is experimental evidence to suggest that oxidative stress mediated by reactive oxygen species (ROS) plays a role in the pathogeneses of myocardial repair/remodeling after MI (7)(8)(9)(10)(11). Oxidative stress results from an oxidant/ antioxidant imbalance: an excess of oxidants relative to antioxidant capacity.…”

Section: Introductionmentioning

confidence: 99%

“…Following MI, NADPH oxidase expression is significantly increased in the infarcted myocardium (21), suggesting that ROS production is enhanced. However, the importance of NADPH oxidase expression on cardiac repair and remodeling remain to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

Cardiac oxidative stress and remodeling following infarction: role of NADPH oxidase

Zhao¹,

Zhao²,

Yan³

et al. 2009

Cardiovascular Pathology

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Background-There is growing recognition that oxidative stress plays a role in the pathogeneses of myocardial repair/remodeling following infarction (MI). NADPH oxidase is a major source for cardiac reactive oxygen species production. Herein, we studied the importance of NADPH oxidase in development of cardiac oxidative stress and its induced molecular and cellular changes related to myocardial repair/remodeling.

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Expression of p22-phox and gp91-phox, Essential Components of NADPH Oxidase, Increases after Myocardial Infarction

Cited by 105 publications

References 30 publications

NADPH oxidase-derived reactive oxygen species in cardiac pathophysiology

NADPH oxidase-derived reactive oxygen species in cardiac pathophysiology

NADPH oxidase signaling and cardiac myocyte function

Cardiac oxidative stress and remodeling following infarction: role of NADPH oxidase

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