Why the study?
Does Nox4 upregulation induce cardiac remodeling and does Nox4 inhibition with GKT137831 attenuate it in a transgenic mouse model?
Population
Cardiac-specific human Nox4 transgenic mice and control mice
Comparison
Angiotensin II infusion and/or treatment with… vs Control mice without AngII infusion or transgene
Design
Preclinical
Key result
Cardiac-specific Nox4 overexpression in mice led to an ≈10-fold increase in Nox4 protein and an 8-fold increase in reactive oxygen species, causing cardiac fibrosis and hypertrophy.
Authors
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Nox4 inhibition may merit testing for remodeling; leaves open translation from mouse overexpression to clinical use.
Does Nox4 upregulation induce cardiac remodeling and does Nox4 inhibition with GKT137831 attenuate it in a transgenic mouse model?
Nox4 upregulation drives cardiac fibrosis and hypertrophy via Akt-mTOR and NFκB pathways, highlighting Nox4 inhibition as a potential therapeutic strategy for cardiac remodeling.
Zhao et al. (2015) studied Cardiac remodeling. Nox4 overexpression (c-hNox4Tg) and Angiotensin II infusion vs. Control mice was evaluated on Cardiac remodeling (fibrosis and hypertrophy). Cardiac-specific Nox4 overexpression in mice led to an ≈10-fold increase in Nox4 protein and an 8-fold increase in reactive oxygen species, causing cardiac fibrosis and hypertrophy.
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