Key result
FGF-23 increases human atrial fibroblast migration ~32% via FGFR1-driven calcium signaling.
Why the study?
Knowledge regarding the effects of FGF-23 on cardiac fibrogenesis remains limited, prompting investigation into whether it modulates cardiac fibroblast activity and its underlying mechanisms.
Does FGF-23 stimulate proliferation and migration in cultured human atrial fibroblasts?
Population
Cultured human atrial fibroblasts
Comparison
FGF-23 (1, 5, and 25 ng/mL) vs control
Design
In vitro controlled laboratory study
Follow-up
48 h
Authors
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Highlights potential FGF-23 role in atrial fibrosis; hypothesis-generating and requires in vivo and clinical validation.
Does FGF-23 stimulate proliferation and migration in cultured human atrial fibroblasts?
p-value: p=<0.05
FGF-23 stimulates human atrial fibroblast proliferation and migration through FGFR1 and PLC-mediated calcium signaling, highlighting a potential mechanism for FGF-23-induced cardiac fibrosis.
Lee et al. (2021) studied Cardiac fibrosis (in vitro model). Fibroblast Growth Factor 23 (FGF-23) vs. Control (untreated cells) was evaluated on Cell proliferation and migration (p=<0.05). FGF-23 at 25 ng/mL significantly increased human atrial fibroblast migration by 32% and proliferation by 17-19% through activation of FGF receptor 1 and PLC/IP3-mediated calcium signaling.
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