Pressure overload-induced myocardial hypertrophy in mice does not require gp91(phox)

Article

关键词: INDUCED CARDIAC-HYPERTROPHY;    NADPH OXIDASE ACTIVITY;    ANGIOTENSIN-II;    NAD(P)H OXIDASE;    FAILING MYOCARDIUM;    HEART-FAILURE;    MYOCYTES;    EXPRESSION;    PATHWAYS;    DISEASE;   

DOI  :  10.1161/01.CIR.0000117229.60628.2F

来源: SCIE

【 摘 要 】

Background - Reactive oxygen species (ROS) may mediate pressure overload - induced myocardial hypertrophy. NADPH oxidase may be involved in this process, because its expression and activity are upregulated by pressure overload and because myocardial hypertrophy caused by a subpressor infusion of angiotensin is attenuated in mice deficient in the gp91(phox) catalytic subunit of NADPH oxidase. Methods and Results - To test the role of NADPH oxidase - dependent ROS in mediating pressure overload - induced myocardial hypertrophy, we subjected transgenic mice lacking gp91phox to chronic pressure overload caused by constriction of the ascending aorta. Contrary to our hypothesis, neither myocardial hypertrophy nor NADPH-dependent superoxide generation was decreased in gp91(phox)-deficient mice after aortic constriction. Aortic constriction caused an exaggerated increase in p22(phox) and p47(phox) mRNA in gp91(phox)-deficient mice. Conclusions - These results indicate that gp91(phox) is not necessary for pressure overload - induced hypertrophy in the mouse and suggest the involvement of another source of ROS, possibly an NADPH oxidase that does not require the gp91(phox) subunit.

【 授权许可】

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