Systemic sclerosis & Raynaud's
Down‐Regulated Fli1 in Scleroderma Myeloid Cells Contributes to Cardiac Fibrosis Via a Galectin‐3/ mTOR Dependent Pathway
Authors' conclusion
Fli1 deficiency in myeloid cells drives Gal-3-dependent activation of mTORC1 in cardiac fibroblasts, promoting cardiac fibrosis and dysfunction in SSc.
Study context
- Population
- Systemic sclerosis (SSc) and control cardiac tissue; myeloid-specific Fli1 knockout mice; human macrophages and primary human cardiac fibroblastscardiac tissue n = 6–7
- Comparison
- SSc vs control tissue/monocytes; myeloid-specific Fli1 knockout vs control mice
- Outcome
- Fli1 and Gal-3 expression in myocardium (immunohistochemistry)
Methodological detailshuman tissue and monocyte analysis, myeloid-specific Fli1 knockout mice (Lyz2Cre/Fli1fl/fl), co-culture experiments
- Human tissue and monocyte analysis
- Myeloid-specific Fli1 knockout mice (Lyz2Cre/Fli1fl/fl)
- Co-culture experiments
Main finding
As reported in the abstract
- Fli1 expression reduced in SSc myocardium vs control (≈6-fold, P = 0.0103)
- Gal-3 increased in SSc myocardium vs control (≈4-fold, P = 0.0031)
Further findings
| Outcome | Estimate | P value |
|---|---|---|
| Mitral E/e' (Lyz2Cre/Fli1fl/fl vs control mice) | mitral E/e' 23.79 ± 8.11 vs 18.76 ± 8.09 | P = 0.04 |
| LV ejection fraction in aged mice (Lyz2Cre/Fli1fl/fl vs control)Aged mice; fibrosis further increased | LV ejection fraction 47.41 ± 5.07 vs 66.15 ± 11.49 | P = 0.0006 |
Original publication
Down‐Regulated Fli1 in Scleroderma Myeloid Cells Contributes to Cardiac Fibrosis Via a Galectin‐3/ mTOR Dependent Pathway. Arthritis Rheumatol. Published 1 September 2026. doi:10.
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