ArticleFrontiers in immunology2025
A20 mRNA therapeutics ameliorate systemic sclerosis by suppressing TRAF-6/NF-KB signaling and DREAM expression and exerting antifibrotic effects.
Article in Frontiers in immunology, 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.
- The ubiquitin-editing enzyme A20 (TNFAIP3): mechanisms of activation, biological function, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- Targeting pyroptosis in periodontitis: mechanisms and therapeutic strategies.Frontiers in immunology · 2026Review
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Authors and funding
13 authors.
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Abstract
Introduction: Systemic sclerosis (SSc) is a chronic autoimmune disorder characterized by progressive fibrosis, vascular abnormalities, and immune dysregulation. Decreased expression of A20 ( Methods: Human dermal fibroblasts were transfected with A20 mRNA -LNP and subsequently stimulated with transforming growth factor-beta (TGF-β). Protein expression levels and fibrotic markers were analyzed by Western blotting and quantitative PCR. In vivo, a bleomycin-induced mouse model of SSc received weekly intramuscular injections of A20 mRNA -LNP. The extent of fibrosis was assessed through histological analysis and immunohistochemistry. Results: Transfection with A20 mRNA-LNP significantly suppressed TRAF6/NF-κB signaling and reduced fibrotic marker expression Discussion: A20 mRNA therapy effectively alleviates fibrosis by restoring A20 expression and inhibiting TRAF6/NF-κB signaling, while also downregulating DREAM, a previously unrecognized target. This dual-pathway regulation underscores the role of A20 and DREAM as central modulators of fibrotic progression. These findings highlight the potential of A20 mRNA-LNP as a novel therapeutic strategy for SSc, offering a multifaceted approach that may surpass current treatment options by simultaneously targeting interconnected pathogenic pathways.
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