Key result
Overexpression of FOXF1 ameliorated angiotensin II-induced cardiac fibrosis in cardiac fibroblasts by inhibiting the TGF-β1/Smad3 signaling pathway.
Why the study?
The molecular mechanisms underlying cardiac fibrosis remain unclear, and whether FOXF1 is involved in its pathogenesis had not been elucidated.
Does FOXF1 overexpression reduce angiotensin II-induced cardiac fibrosis in cardiac fibroblasts?
Population
Ang II-induced cardiac fibroblasts
Comparison
FOXF1 overexpression vs control
Design
In vitro controlled experimental study
Authors
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In vitro data position FOXF1 as a potential antifibrotic target; leaves open in vivo efficacy and clinical translation.
Does FOXF1 overexpression reduce angiotensin II-induced cardiac fibrosis in cardiac fibroblasts?
FOXF1 overexpression attenuates angiotensin II-induced cardiac fibrosis in vitro, suggesting it may serve as a novel therapeutic target for pathological cardiac fibrosis.
Jin et al. (2020) studied Cardiac fibrosis. Overexpression of FOXF1 was evaluated on Proliferation, migration, oxidative stress, and extracellular matrix production in cardiac fibroblasts. Overexpression of FOXF1 ameliorated angiotensin II-induced cardiac fibrosis in cardiac fibroblasts by inhibiting the TGF-β1/Smad3 signaling pathway.
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