Systemic sclerosis & Raynaud's
Fibroblast Mitochondrial Ca 2+ Overload Drives Skin Fibrosis via Mitochondrial DNA Leakage and Cyclic GMP ‐ AMP Synthase–Stimulator of Interferon Genes Activation in Systemic Sclerosis
Authors' conclusion
The Ca2+-mtDNA-cGAS-STING axis drives fibroblast activation and skin fibrosis in SSc, representing a promising therapeutic target.
Study context
- Population
- Patients with systemic sclerosis (SSc) and healthy controls; primary dermal fibroblasts from dcSSc patients and healthy controls (HCs); bleomycin-induced skin fibrosis micen = 6 mice per group
- Comparison
- SSc vs HCs
- Outcome
- Plasma mtDNA levels and mechanism by which mtDNA leakage drives fibroblast activation
Methodological detailscase-control plasma analysis, in vitro primary dermal fibroblasts, bleomycin-induced skin fibrosis mouse model
- Case-control plasma analysis
- In vitro primary dermal fibroblasts
- Bleomycin-induced skin fibrosis mouse model
Main finding
As reported in the abstract
Correlation of plasma mitochondrial DNA (mtDNA) with FVC
r = −0.436
P < 0.01
Correlation of plasma mtDNA with mRSS
r = 0.807
P < 0.001
Correlation of plasma mtDNA with IL-6
r = 0.667
P < 0.001
Correlation of plasma mtDNA with TGF-β
r = 0.678
P < 0.001
Parts of this Brief are withheld: the automatic checks could not confirm them against the abstract.
Original publication
Fibroblast Mitochondrial Ca 2+ Overload Drives Skin Fibrosis via Mitochondrial DNA Leakage and Cyclic GMP ‐ AMP Synthase–Stimulator of Interferon Genes Activation in Systemic Sclerosis. Arthritis Rheumatol. Published 23 June 2026. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →