ArticleACR open rheumatology2025
Understanding Cardiovascular Events With JAK Inhibitors: Tofacitinib Reduces Synovial and Vascular Inflammation but not the Prothrombotic Effects of Inflammatory Cytokines on Endothelium.
Article in ACR open rheumatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Positive and Negative Cardiovascular Effects of JAK Inhibitors in Inflammation.ACR open rheumatology · 2026Review
- Metabolic-Epigenetic Crosstalk in Takayasu Arteritis: The ANK2-MAVS-IL-8 Axis as a Novel Therapeutic Paradigm.International journal of molecular sciences · 2026Review
- Perioperative Management of Biologic and Targeted Synthetic DMARDs in Orthopedic Surgery: Balancing Infection Risk and Disease Control.Microorganisms · 2026Review
- Ulcerative colitis (UC) in the elderly: diagnostic and therapeutic considerations.Frontiers in aging · 2026Review
- Inflammasome-associated pyroptosis and tumor angiogenesis in prostate cancer.Iranian journal of basic medical sciences · 2026Review
- Effects of treatment with janus kinase inhibitors on coronary microvascular perfusion in patients with rheumatoid arthritis: an observational prospective cohort study.Rheumatology international · 2025Observational
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveInflammation drives cardiovascular disease in rheumatoid arthritis (RA). Treatment with tofacitinib, a JAK1/JAK3 inhibitor, is associated with increased cardiovascular events in patients with RA. Here, we determined its effects on cytokine production during interactions between immune cells at the synovial and vascular levels and its impact on endothelial activation and coagulation during inflammation.
methodsActivated human peripheral blood mononuclear cells (PBMCs) were cocultured with RA synoviocytes or endothelial cells (ECs) mimicking the cellular interactions in synovium and vessels responsible for cytokine production. A dose-response of tofacitinib was tested on interferon γ, interleukin (IL) 17A, IL-10, IL-6, and IL-1β, and cytokine production was measured by enzyme-linked immunosorbent assay at 48 hours. Endothelial activation was induced with IL-17A and tumor necrosis factor (TNF) or on contact with PBMCs. Shortly after tofacitinib treatment, the expression of EC activation markers, specifically IL-6, IL-8, vascular cell adhesion molecule 1 (VCAM-1), and E-selectin, and of coagulation, including tissue factor and thrombomodulin, was assessed by real-time polymerase chain reaction.
resultsTofacitinib differentially inhibited production of IFNɣ, IL-17A, and IL-10 from PBMC cocultures with RA synoviocytes or ECs (all P < 0.001). In cocultures with ECs, tofacitinib reduced further IL-6 and IL-8 production (both P < 0.001). In ECs activated by TNF/IL-17A or indirectly via contact with activated PBMCs, tofacitinib decreased IL-6 upregulation but not that of IL-8, E-selectin, or tissue factor. Thrombomodulin was significantly decreased. VCAM-1 was greatly induced with a higher dose of tofacitinib in ECs incubated directly with added inflammatory cytokines (P < 0.05) or released by interaction with activated PBMCs (P < 0.001).
conclusionTofacitinib inhibits synovium and vascular inflammation but fails to prevent the prothrombotic effects of inflammatory cytokines on ECs.
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