Involvement of NADPH oxidases in cardiac remodelling and heart failure.
Cardiac remodelling occurs in response to stress, such as chronic hypertension or myocardial infarction, and forms the substrate for subsequent development of heart failure. Key pathophysiological features include ventricular hypertrophy, interstitial fibrosis, contractile dysfunction, and chamber dilatation. Although the molecular mechanisms are complex and not fully defined, substantial evidence now implicates increased oxidative stress as being important. The NADPH oxidase ('Nox') enzymes are a particularly important source of reactive oxygen species that are implicated in redox signalling. This article reviews the evidence for an involvement of NADPH oxidases in different aspects of adverse cardiac remodelling. A better understanding of the roles of this complex enzyme family may define novel therapeutic targets for the prevention of heart failure.
Sirker
Alexander
A
Cardiovascular Division, Department of Cardiology, King's College London School of Medicine, London, UK.
Zhang
Min
M
Murdoch
Colin
C
Shah
Ajay M
AM
D000818:Animals; D017209:Apoptosis; D006332:Cardiomegaly / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D005355:Fibrosis; D006333:Heart Failure / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D009200:Myocardial Contraction / Q000502:physiology; D009203:Myocardial Infarction / Q000503:physiopathology; D019255:NADPH Oxidases / Q000378:metabolism*; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction; D020257:Ventricular Remodeling / Q000502:physiology*
D017382:Reactive Oxygen Species; D019255:NADPH Oxidases