Key result
Nox4 knockdown, DPI, and the Nox1/4 dual inhibitor GKT137831 attenuated Angiotensin-II-induced mouse cardiac fibroblast proliferation and migration.
Why the study?
Does Nox4 inhibition or knockdown prevent Angiotensin-II-induced proliferation and migration in adult mouse cardiac fibroblasts?
Population
Adult mouse cardiac fibroblasts (CF)
Comparison
Nox4 knockdown, Nox inhibitor DPI, Nox1/Nox4… vs Control or Angiotensin-II alone
Design
Preclinical
Authors
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No immediate clinical implications for hypertensive heart disease; leaves open Nox4/IL-18 as mechanistic targets for further study.
Does Nox4 inhibition or knockdown prevent Angiotensin-II-induced proliferation and migration in adult mouse cardiac fibroblasts?
Inhibition of Nox4 or the AT1/Nox4 interaction attenuates Angiotensin-II-induced cardiac fibroblast proliferation and migration, highlighting a potential therapeutic target for chronic hypertension-induced adverse cardiac remodeling.
Somanna et al. (2015) studied Angiotensin-II-induced cardiac fibroblast proliferation and migration. Nox4 knockdown, DPI, or GKT137831 was evaluated on Cardiac fibroblast proliferation and migration. Nox4 knockdown, DPI, and the Nox1/4 dual inhibitor GKT137831 attenuated Angiotensin-II-induced mouse cardiac fibroblast proliferation and migration.
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