Why the study?
Does targeted disruption of the NADPH oxidase subunit gp91(phox) prevent angiotensin II-induced cardiac hypertrophy in mice?
Population
Mice with targeted disruption of the NADPH oxidase subunit gp91 (gp91) and matched wild-type mice
Comparison
Subcutaneous angiotensin II infusion at a… vs Wild-type mice compared to gp91 mice, both…
Design
Preclinical
Follow-up
2 weeks
Authors
Loading...
Animal data preclude clinical translation; leaves open gp91(phox) as a therapeutic target in human hypertrophy.
Does targeted disruption of the NADPH oxidase subunit gp91(phox) prevent angiotensin II-induced cardiac hypertrophy in mice?
This study demonstrates that a gp91(phox)-containing NADPH oxidase is essential for the development of angiotensin II-induced cardiac hypertrophy, independent of blood pressure changes.
Bendall et al. (2002) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: