Systemic sclerosis & Raynaud's
Targeting Prostaglandin D2 synthase (PTGDS) inhibits pro-inflammatory fibroblasts associated with skin fibrosis in systemic sclerosis
Authors' conclusion
PTGDS-induced pro-inflammatory fibroblasts caused Th2 cell infiltration and skin fibrosis. Inhibition of PTGDS attenuated the inflammation and fibrosis in the skin.
Study context
- Population
- Skin tissues from systemic sclerosis (SSc) patients; PTGDS-overexpressed BJ cells; Bleomycin (BLM)-induced skin fibrosis mouse model
Methodological detailsbioinformatics, in vitro, bleomycin-induced skin fibrosis mouse model
- Bioinformatics
- In vitro
- Bleomycin-induced skin fibrosis mouse model
Main finding
As reported in the abstract
- PTGDS expression significantly elevated in dermal fibroblasts of SSc patients
- In vitro, PTGDS overexpression upregulated various chemokines in skin fibroblasts, enhancing migration of CD4+ T cells, particularly Th2; reversed by PTGDS inhibitor AT56
- PTGDS-overexpressed fibroblasts promoted Th2 cell infiltration and skin fibrosis
- Oral AT56 significantly attenuated BLM-induced skin inflammation and fibrosis in vivo
Original publication
Targeting PTGDS inhibits pro-inflammatory fibroblasts associated with skin fibrosis in systemic sclerosis. Rheumatology (Oxford). Published 6 June 2025. doi:10. 1093/ rheumatology/ keaf276
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