Key result
Inhibiting endothelial cell junctional instability and vascular leakage with the synthetic metabolite UAS03 effectively mitigated ANGPTL2-driven vasculopathy and inhibited fibrogenesis in a mouse model of systemic sclerosis.
Why the study?
Vasculopathy is a common hallmark of fibrotic disorders including systemic sclerosis, but its underlying etiology and contribution to fibrogenesis remain ill defined.
Does UAS03 mitigate vasculopathy and inhibit fibrogenesis in a mouse model of systemic sclerosis?
Population
Snail transgenic mouse model of systemic sclerosis and endothelial cells
Comparison
Treatment with synthetic analog of microbial metabolite Urolithin A (UAS03)
Design
Preclinical animal and cellular study
Authors
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Hypothesis-generating for UAS03 in systemic sclerosis; human validation required before clinical consideration.
Does UAS03 mitigate vasculopathy and inhibit fibrogenesis in a mouse model of systemic sclerosis?
Inhibiting ANGPTL2-driven endothelial cell junctional instability with UAS03 mitigates vasculopathy and fibrogenesis in a mouse model of systemic sclerosis.
Saha et al. (2025) studied Systemic sclerosis. UAS03 vs. Vehicle control was evaluated on Vascular leakage and dermal thickness. Inhibiting endothelial cell junctional instability and vascular leakage with the synthetic metabolite UAS03 effectively mitigated ANGPTL2-driven vasculopathy and inhibited fibrogenesis in a mouse model of systemic sclerosis.
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