Lupus & antiphospholipid syndrome
Plasma exosomal fibroblast activation protein: a novel biomarker links fatty acid metabolic dysregulation to systemic lupus erythematosus
Authors' conclusion
We identify plasma exosomal FAP as a novel biomarker linking fatty acid metabolic dysregulation to SLE.
Study context
- Population
- Patients with active systemic lupus erythematosus (SLE), inactive SLE, rheumatoid arthritis (RA) and healthy controls
- Comparison
- Active SLE vs inactive SLE vs RA vs healthy controls
- Outcome
- Circulating biomarkers within plasma exosomes linking fatty acid metabolic rewiring to SLE pathogenesis
Methodological detailscase-control, proteomic and metabolomic profiling (liquid chromatography-mass spectrometry (LC-MS)), validation by nanoflow cytometry and targeted metabolomics
- Case-control
- Proteomic and metabolomic profiling (LC-MS)
- Validation by nanoflow cytometry and targeted metabolomics
Main finding
As reported in the abstract
- Marked enrichment of fibroblast activation protein (FAP) in plasma exosomes from SLE patients, highest in active SLE
- Plasma exosomal FAP specifically increased in SLE but not RA (nanoflow cytometry)
- SLE plasma exosomes: increased saturated (palmitic acid, etc) and ω-6 polyunsaturated fatty acids (PUFAs) (arachidonic acid (AA), etc), decreased ω-3 PUFAs (α-linolenic acid, eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), etc)
- Active SLE: AA/DHA and total ω-6/ω-3 ratios significantly elevated, EPA/AA ratio reduced
- Exosomal FAP correlated positively with SLEDAI-2000 and pro-inflammatory fatty acid profiles (AA, total ω-6, AA/DHA), negatively with anti-inflammatory profiles (DHA, EPA, total ω-3, EPA/AA)
Original publication
Plasma exosomal fibroblast activation protein: a novel biomarker links fatty acid metabolic dysregulation to systemic lupus erythematosus. Arthritis Res Ther. Published 30 March 2026. doi:10.
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