Key result
Treatment with A2AR antagonists Istradefylline and ZM241385 reduced oxidative stress and decreased the expression of fibrotic markers including collagen1a1, BGN, and α-SMA in TGF-β-stimulated cardiac fibroblasts.
Why the study?
To investigate the possible crosstalk between A2AR and biglycan modulation in an in vitro model of TGF-β-induced cardiac fibrosis.
Population
Immortalized human cardiac fibroblasts stimulated with TGF-β
Comparison
Istradefylline vs ZM241385 vs untreated TGF-β-challenged cells
Design
In vitro controlled laboratory study
Follow-up
24 h
Authors
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BGN may regulate fibroblast phenotype in fibrosis; hypothesis-generating for targeted therapies, clinical translation unproven.
A2AR antagonism attenuates TGF-β-induced fibrotic processes and oxidative stress in human cardiac fibroblasts, highlighting a potential therapeutic target for pathological cardiac remodeling.
Scuruchi et al. (2023) studied Cardiac fibrosis. A2AR antagonists (Istradefylline and ZM241385) vs. TGF-β-challenged human fibroblasts without A2AR antagonist was evaluated on Oxidative stress (ROS reduction) and gene/protein expression of fibrotic markers. Treatment with A2AR antagonists Istradefylline and ZM241385 reduced oxidative stress and decreased the expression of fibrotic markers including collagen1a1, BGN, and α-SMA in TGF-β-stimulated cardiac fibroblasts.
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