Lupus & antiphospholipid syndrome
Reactive Oxygen Species–Induced Modifications of Fibrin Clots as a Link Between Immune Responses and Atherothrombosis in Systemic Lupus Erythematosus
Authors' conclusion
Oxidative stress may drive structural and functional modifications of fibrinogen in SLE, potentially acting as a novel pathogenetic mechanism in atherothrombosis among these patients.
Study context
- Population
- Adult patients with systemic lupus erythematosus (SLE) and matched controls
- Participants
- 144 vs 90
- Exposure
- Patients with SLE vs matched controls
- SLEn = 144
- Controlsn = 90reference
Methodological detailsmatched controls, in vitro mechanistic experiments
- Matched controls
- In vitro mechanistic experiments
Main finding
As reported in the abstract
- Increased leukocyte reactive oxygen species (ROS) production in SLE, mainly due to neutrophil NADPH oxidase activation
- Renal biopsies with active proliferative LN: overexpression of NADPH oxidase complex p22phox
- Plasma oxidative stress: elevated plasma lipid peroxidation and reduced antioxidant defenses
- Fibrinogen oxidation associated with denser fibrin networks, lower clot porosity and reduced susceptibility to plasmin-mediated fibrin lysis
- Fibrinogen modifications correlated with redox status alterations and disease activity
Observational data: associations, not effects.
Original publication
Reactive Oxygen Species–Induced Modifications of Fibrin Clots as a Link Between Immune Responses and Atherothrombosis in Systemic Lupus Erythematosus. Arthritis Rheumatol. Published 28 December 2025. doi:10.
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