Key result
Loss of the p47phox subunit or Ang 1-7 supplementation in ACE2 knockout mice normalized increased NADPH oxidase activity, superoxide production, and systolic dysfunction following pressure overload.
Why the study?
Does loss of p47phox or Ang 1-7 supplementation prevent enhanced susceptibility to biomechanical stress and heart failure in ACE2 null mice?
Population
Wild-type (Ace2), ACE2 knockout (ACE2KO, Ace2), p47 knockout (p47KO, p47), and ACE2/p47 double KO mice…
Comparison
Loss of p47phox or Ang 1-7 supplementation vs ACE2KO mice without p47phox loss or Ang 1-7…
Design
Preclinical
Authors
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Should not change clinical practice in heart failure; extends mechanistic evidence for p47phox and Ang 1-7 in ACE2-deficient models.
Does loss of p47phox or Ang 1-7 supplementation prevent enhanced susceptibility to biomechanical stress and heart failure in ACE2 null mice?
In ACE2-deficient mice, biomechanical stress activates the myocardial NADPH oxidase system via the p47phox subunit, leading to adverse remodeling that can be prevented by p47phox deletion or Ang 1-7 supplementation.
Bodiga et al. (2011) studied Pressure overload-induced heart failure. Loss of p47phox (double knockout) or Ang 1-7 supplementation vs. ACE2 knockout mice and wild-type mice was evaluated on Changes in peptide levels, NADPH oxidase activity, gene expression, MMP activity, pathological signalling, and heart function. Loss of the p47phox subunit or Ang 1-7 supplementation in ACE2 knockout mice normalized increased NADPH oxidase activity, superoxide production, and systolic dysfunction following pressure overload.
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