Systemic sclerosis & Raynaud's
Tumour necrosis factor-like weak inducer of apoptosis participates in the development of cutaneous fibrosis in an experimental systemic sclerosis model
Authors' conclusion
These findings demonstrate that the TWEAK/Fn14 signalling axis contributes to SSc progression by exacerbating local inflammation and fibrosis.
Study context
- Population
- Skin tissue from systemic sclerosis (SSc) patients and a bleomycin (BLM)-induced mouse model
- Comparison
- Exogenous TWEAK or Fn14 antagonist in BLM-induced SSc mouse model; TWEAK/Fn14 expression in SSc skin
- Outcome
- Role of TWEAK/Fn14 signalling in SSc skin fibrosis
Methodological detailshuman SSc skin tissue, BLM-induced mouse model, Immunohistochemistry staining, Western blotting and hydroxyproline content detection
- Human SSc skin tissue
- BLM-induced mouse model
- Immunohistochemistry staining, Western blotting and hydroxyproline content detection
Main finding
As reported in the abstract
- TWEAK and Fn14 markedly elevated in SSc cutaneous lesions
- In SSc mouse model, exogenous TWEAK partially exacerbated cutaneous fibrosis and inflammatory cell infiltration
- Fn14 antagonist significantly reduced BLM-induced histological changes in the skin
Original publication
Tumour necrosis factor-like weak inducer of apoptosis participates in the development of cutaneous fibrosis in an experimental systemic sclerosis model. Clin Exp Rheumatol. Published 6 August 2024. doi:10.
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