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Pressure overload-induced myocardial hypertrophy in mice does not require gp91phox
Melanie Maytin1, Deborah A Siwik, Masahiro Ito
1Department of Medicine, Cardiovascular Section, Boston University Medical Center, and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Mass 02118, USA.
Circulation
|February 26, 2004
Summary
This study found that the gp91phox subunit is not essential for pressure overload-induced myocardial hypertrophy. Alternative NADPH oxidase sources may contribute to this cardiac response.
Area of Science:
- Cardiovascular Biology
- Oxidative Stress Research
- Molecular Cardiology
Background:
- Reactive oxygen species (ROS) are implicated in pressure overload-induced myocardial hypertrophy.
- NADPH oxidase, a key source of ROS, is upregulated by pressure overload.
- Previous studies suggested gp91phox subunit involvement in angiotensin-induced hypertrophy.
Purpose of the Study:
- To investigate the role of NADPH oxidase-dependent ROS in mediating pressure overload-induced myocardial hypertrophy.
- To determine if gp91phox deficiency protects against cardiac hypertrophy.
Main Methods:
- Utilized transgenic mice lacking the gp91phox subunit.
- Subjected mice to chronic pressure overload via aortic constriction.
- Assessed myocardial hypertrophy and NADPH-dependent superoxide generation.
Main Results:
- gp91phox-deficient mice did not show reduced myocardial hypertrophy after aortic constriction.
- NADPH-dependent superoxide generation was not decreased in knockout mice.
- Aortic constriction led to increased p22phox and p47phox mRNA in gp91phox-deficient mice.
Conclusions:
- The gp91phox subunit is not required for pressure overload-induced myocardial hypertrophy in mice.
- These findings suggest alternative ROS sources, potentially other NADPH oxidase isoforms, mediate cardiac hypertrophy.
- Further research is needed to identify non-gp91phox NADPH oxidase involvement.
