ArticleArthritis research & therapy2025
Baricitinib ameliorates skin fibrosis via direct fibroblast suppression and endothelial exosome-mediated paracrine signaling.
Article in Arthritis research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Decoding fibroblast activation: Transcriptional networks in hepatic stellate cells and across fibrotic organs (Review).International journal of molecular medicine · 2026Review
- Refractory IgG4-related skin disease successfully treated with intravenous methylprednisolone and baricitinib.JAAD case reports · 2026Article
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Authors and funding
4 authors.
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Abstract
backgroundNovel therapies are urgently needed for diffuse cutaneous systemic sclerosis (dcSSc). Aberrant JAK/STAT signaling drives fibrosis, but JAK inhibitors’ effects on vascular pathology and potential synergy with endothelial-derived exosomes remain unclear.
methodsUtilizing bleomycin (BLM)-induced human skin fibroblast (HSF) activation and hypoxia-impaired human umbilical vein endothelial cell (HUVEC) models, we investigated the anti-fibrotic mechanisms of the JAK1/JAK2 inhibitor Baricitinib. Functional assays assessed proliferation, migration, tube formation, extracellular matrix (ECM) deposition, and cytokine production. Conditioned media (CM) and exosomes from Baricitinib-treated HUVECs were applied to BLM-HSFs to evaluate paracrine/exosomal roles.
resultsBaricitinib (6 nmol/L) directly inhibited BLM-induced HSF proliferation, Collagen I/III, α-SMA expression, and actin polymerization. In hypoxia-damaged HUVECs, Baricitinib (54 nmol/L) restored proliferation, migration, tube formation, and suppressed JAK/STAT3 hyperactivation. Crucially, CM from Baricitinib-treated HUVECs significantly attenuated BLM-HSF fibrotic activation, an effect abolished by exosome inhibitor GW4869. Exosomes from Baricitinib-treated HUVECs exhibited enhanced uptake by HSFs and superior suppression of proliferation, cytoskeletal reorganization, and profibrotic marker expression compared to control exosomes; these effects were diminished by exosome disruption.
conclusionBaricitinib alleviates skin fibrosis via a dual mechanism: direct suppression of fibroblast activation and indirect mitigation through the “reprogramming” of HUVEC-derived exosomes. By rescuing endothelial dysfunction and enhancing the anti-fibrotic cargo of endothelial exosomes, Baricitinib interrupts the vascular damage-fibrosis cycle in dcSSc. This identifies endothelial exosomes as key mediators of JAK inhibitor efficacy, offering a novel therapeutic paradigm.
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