Literature summary for 1.6.3.1 extracted from

Doerries, C.; Grote, K.; Hilfiker-Kleiner, D.; Luchtefeld, M.; Schaefer, A.; Holland, S.M.; Sorrentino, S.; Manes, C.; Schieffer, B.; Drexler, H.; Landmesser, U.
Critical role of the NAD(P)H oxidase subunit p47phox for left ventricular remodeling/dysfunction and survival after myocardial infarction (2007), Circ. Res., 100, 894-903.

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Application

Application	Comment	Organism
medicine	after myocardial infarction, NAD(P)H oxidase activity is markedly increased in remote left ventricular myocardium of wild-type mice but not in mice deficient in subunit p47phox. Increased myocardial xanthine oxidase activity is observed in wild-type, but not in p47phox-deficient mice after myocardial infarction. Left ventricular cavity dilatation and dysfunction 4 weeks after infarction are markedly attenuated in p47phox-deficient mice and cardiomyocyte hypertrophy, apoptosis, and interstitial fibrosis are substantially reduced as compared with wild-type. The survival rate is markedly higher in mice deficient in subunit p47phox	Mus musculus

Organism

Organism	UniProt	Comment	Textmining
Mus musculus	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
heart	after myocardial infarction, NAD(P)H oxidase activity is markedly increased in remote left ventricular myocardium of wild-type mice but not in mice deficient in subunit p47phox. Increased myocardial xanthine oxidase activity is observed in wild-type, but not in p47phox-deficient mice after myocardial infarction. Left ventricular cavity dilatation and dysfunction 4 weeks after infarction are markedly attenuated in p47phox-deficient mice and cardiomyocyte hypertrophy, apoptosis, and interstitial fibrosis are substantially reduced as compared with wild-type. The survival rate is markedly higher in mice deficient in subunit p47phox	Mus musculus	-

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Release 2023.1 (January 2023)