TY - JOUR
T1 - NADPH oxidase and heart failure
AU - Murdoch, Colin E.
AU - Grieve, David J.
AU - Cave, Alison C.
AU - Looi, Yee Hoo
AU - Shah, Ajay M.
PY - 2006/4
Y1 - 2006/4
N2 - Reactive oxygen species play important roles in the pathophysiology of chronic heart failure secondary to chronic left ventricular hypertrophy or myocardial infarction. Reactive oxygen species influence several components of the phenotype of the failing heart, including contractile function, interstitial fibrosis, endothelial dysfunction and myocyte hypertrophy. Recent studies implicate the production of reactive oxygen species by a family of NADPH oxidases in these effects. NADPH oxidases are activated in an isoform-specific manner by many pathophysiological stimuli and exert distinct downstream effects. Understanding NADPH oxidase activation and regulation, and their downstream effectors, could help to develop novel therapeutic targets.
AB - Reactive oxygen species play important roles in the pathophysiology of chronic heart failure secondary to chronic left ventricular hypertrophy or myocardial infarction. Reactive oxygen species influence several components of the phenotype of the failing heart, including contractile function, interstitial fibrosis, endothelial dysfunction and myocyte hypertrophy. Recent studies implicate the production of reactive oxygen species by a family of NADPH oxidases in these effects. NADPH oxidases are activated in an isoform-specific manner by many pathophysiological stimuli and exert distinct downstream effects. Understanding NADPH oxidase activation and regulation, and their downstream effectors, could help to develop novel therapeutic targets.
UR - http://www.scopus.com/inward/record.url?scp=33644835876&partnerID=8YFLogxK
U2 - 10.1016/j.coph.2005.10.008
DO - 10.1016/j.coph.2005.10.008
M3 - Article
AN - SCOPUS:33644835876
SN - 1471-4892
VL - 6
SP - 148
EP - 153
JO - Current Opinion in Pharmacology
JF - Current Opinion in Pharmacology
IS - 2
ER -