ArticleClinical rheumatology2024
JAK inhibitors inhibit angiogenesis by reducing VEGF production from rheumatoid arthritis-derived fibroblast-like synoviocytes.
Article in Clinical rheumatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Reticuline alleviates rheumatoid arthritis by suppressing the JAK/STAT signaling pathway.Clinical rheumatology · 2026Article
- Fibroblast-like Synoviocytes as Therapeutic Targets in Rheumatoid Arthritis: Current Evidence on DMARD-Mediated Modulation.Biomedicines · 2026Review
- Bioinformatics-driven single-cell sequencing analysis of angiogenesis-related genes in rheumatoid arthritis.Frontiers in immunology · 2026Article
- Endothelial cell-targeting aptamer-empowered exosomes accelerate wound healing by promoting specialized angiogenesis in type 1 diabetic mice.Stem cell research & therapy · 2025Article
- Antibiotics for Rheumatologic Diseases: A Critical Review.International journal of molecular sciences · 2025Review
- Systematic validation of miR-503-5p abnormal expression in diabetic vascular complications: a meta-analysis and exploration of its targeted regulatory mechanism in retinopathy.Diabetology & metabolic syndrome · 2025Article
- Ectopic Nociceptor Sprouting as a Key Peripheral Driver of Pain in Rheumatoid Arthritis.Current rheumatology reports · 2025Review
- Unveiling the Therapeutic Potential: Targeting Fibroblast-like Synoviocytes in Rheumatoid Arthritis.Expert reviews in molecular medicine · 2025Review
- Comparison of anti-inflammatory and anti-angiogenic effects of JAK inhibitors in IL-6 and TNFα-stimulated fibroblast-like synoviocytes derived from patients with RA.Scientific reports · 2025Article
- Article
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13 authors.
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Abstract
INTRODUCTION/
objectivesJAK/STAT signaling inhibition exerts therapeutic effects on angiogenesis in rheumatoid arthritis (RA). However, whether the inhibitory effect differs among JAK inhibitors because of differing selectivity is unknown. Therefore, we compared the inhibitory effects of tofacitinib, baricitinib, peficitinib, upadacitinib, and filgotinib on angiogenesis.
methodRA-derived fibroblast-like synoviocytes (RA-FLS) were seeded on type I collagen gel, and human umbilical vein endothelial cells (HUVECs) were directly added. The control and aforementioned JAK inhibitors were added to the medium, followed by stimulation with interleukin (IL)-6 and soluble IL-6 receptor (sIL-6R). Each JAK inhibitor's concentration was determined based on estimated blood concentrations. The vascular endothelial growth factor (VEGF) concentration was evaluated with an enzyme-linked immunosorbent assay using the medium from the first exchange. A migration assay was performed, and HUVEC migration was evaluated using CD31 fluorescence immunostaining.
resultsHematoxylin-eosin staining showed that compared with the non-JAKi treatment group, the JAKi treatment group markedly degenerated in the sub-lining and deep lining, with decreased lymphocyte infiltration and neovascularization [Rooney's score subscale, non-JAKi vs JAKi (median, 6.5 vs 2.5, p = 0.005)]. In vitro, IL-6 and sIL-6R administration increased VEGF production from RA-FLS and promoted neovascularization in HUVECs, and JAK-inhibitor administration, which decreased VEGF production from RA-FLS and suppressed HUVEC migration, inhibited neovascularization in RA-FLS and HUVEC co-cultures.
conclusionsThe JAK inhibitors suppressed IL-6-induced angiogenesis via decreased VEGF production and HUVEC migration in RA-FLS and HUVEC co-cultures. No significant differences were observed among the JAK inhibitors, whose anti-angiogenic effect may be an important mechanism for RA treatment. Key Points • JAK inhibitors inhibit angiogenesis in RA by reducing VEGF production from RA-derived fibroblast-like synoviocytes. • Our study provides new insights into RA treatment by elucidating the anti-angiogenic effect of JAK inhibitors.
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