Key result
FGF-2 effectively blocks TGF-β1-mediated myofibroblast activation in aortic valvular interstitial cells by preventing the nuclear localization of Smad transcription factors via a MAPK-dependent pathway.
Population
Valvular interstitial cells isolated from porcine aortic valve leaflets and intact porcine aortic leaflet…
Comparison
Basic fibroblast growth factor at various… vs Untreated controls, TGF-beta1 treatment alone…
Design
Preclinical
Follow-up
48 to 96 hours for cell cultures; 2 weeks for valve…
Authors
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Hypothesis-generating for antifibrotic targets in aortic valve disease; leaves open translation from cell models to clinical therapies.
FGF-2 prevents TGF-beta1-mediated myofibroblast activation and calcification in valvular interstitial cells, identifying a potential signaling pathway to target for the treatment of fibrotic valvular heart disease.
Cushing et al. (2008) studied Valvular fibrosis. FGF-2 (basic fibroblast growth factor) vs. Untreated controls or TGF-β1 alone was evaluated on Myofibroblast activation (α-SMA expression, Smad activity, matrix deposition). FGF-2 effectively blocks TGF-β1-mediated myofibroblast activation in aortic valvular interstitial cells by preventing the nuclear localization of Smad transcription factors via a MAPK-dependent pathway.
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