ArticleCellular & molecular immunology2024
Metabolic reprogramming by Syntenin-1 directs RA FLS and endothelial cell-mediated inflammation and angiogenesis.
Article in Cellular & molecular immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Systematic Review of Interleukin-35 in Endothelial Dysfunction: A New Target for Therapeutic Intervention.Mediators of inflammation · 2025Pooled it
- Engineering autoimmune disease models using organoids: Harnessing microenvironmental engineering for precision medicine and immunological recapitulation.Bioengineering & translational medicine · 2026Review
- Integrated network toxicology and bioinformatics approaches explore potential mechanisms linking organophosphate flame retardant exposure to rheumatoid arthritis.Molecular diversity · 2026Article
- Article
- Beyond PAD Inhibition: Emerging Avenues and Natural Products for Targeting Citrullination in Immune Diseases.Biomedicines · 2026Review
- Tofacitinib repairs inflammation and mitochondrial dysregulation in GM-CSF-reprogrammed RA macrophages.Cellular & molecular immunology · 2026Article
- Mechanical Strain-Programmed SDC1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Fraxin Attenuates Rheumatoid Arthritis by Regulating Macrophage Polarization and Inhibiting Fibroblast-like Synoviocyte Proliferation.International journal of molecular sciences · 2026Article
- Identification of SDC1 as a Key Regulator and Therapeutic Target in Rheumatoid Arthritis via JAK2-STAT3 Pathway.International journal of rheumatic diseases · 2026Article
- The protection of mesenchymal stem cells in metabolic reprogramming and endothelial-mesenchymal transition in diabetic aortas.Stem cells translational medicine · 2026Article
- From Systemic Autoimmunity to the Local Immune Niche of the Synovium: New Insights into the Development of Rheumatoid Arthritis.Journal of inflammation research · 2026Review
- Metabolic control of RNA methylation in rheumatoid arthritis: from synovial stress to pathogenic cellular adaptation.Frontiers in immunology · 2026Review
- Roles of immune cell metabolism in rheumatoid arthritis.Frontiers in immunology · 2026Review
- Immunometabolic dysregulation in autoimmune rheumatic diseases: the central role of glycolytic reprogramming in pathogenesis and traditional Chinese medicine therapy.Frontiers in immunology · 2026Review
- Mitochondrial fission and fusion in inflammatory diseases: mechanisms and therapeutic implications.Journal of translational medicine · 2025Review
- Research Progress Regarding the Use of Single-Cell Sequencing Technology in Analyzing Tumor Endothelial Cell Pathophysiology.International journal of molecular sciences · 2025Review
- GRK2-mediated phosphorylation and de-succinylation of PKM2 reduce macrophage glycolysis in rheumatoid arthritis.Acta pharmacologica Sinica · 2025Article
- Angiogenesis in rheumatoid Arthritis: Pathological characterization, pathogenic mechanisms, and nano-targeted therapeutic strategies.Bioactive materials · 2025Review
- Near-infrared light-driven metabolic reprogramming of synoviocytes for the treatment of rheumatoid arthritis.Nature communications · 2025Article
- IGF2BP3-mediated mBone research · 2025Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
Abstract
A novel rheumatoid arthritis (RA) synovial fluid protein, Syntenin-1, and its receptor, Syndecan-1 (SDC-1), are colocalized on RA synovial tissue endothelial cells and fibroblast-like synoviocytes (FLS). Syntenin-1 exacerbates the inflammatory landscape of endothelial cells and RA FLS by upregulating transcription of IRF1/5/7/9, IL-1β, IL-6, and CCL2 through SDC-1 ligation and HIF1α, or mTOR activation. Mechanistically, Syntenin-1 orchestrates RA FLS and endothelial cell invasion via SDC-1 and/or mTOR signaling. In Syntenin-1 reprogrammed endothelial cells, the dynamic expression of metabolic intermediates coincides with escalated glycolysis along with unchanged oxidative factors, AMPK, PGC-1α, citrate, and inactive oxidative phosphorylation. Conversely, RA FLS rewired by Syntenin-1 displayed a modest glycolytic-ATP accompanied by a robust mitochondrial-ATP capacity. The enriched mitochondrial-ATP detected in Syntenin-1 reprogrammed RA FLS was coupled with mitochondrial fusion and fission recapitulated by escalated Mitofusin-2 and DRP1 expression. We found that VEGFR1/2 and Notch1 networks are responsible for the crosstalk between Syntenin-1 rewired endothelial cells and RA FLS, which are also represented in RA explants. Similar to RA explants, morphological and transcriptome studies authenticated the importance of VEGFR1/2, Notch1, RAPTOR, and HIF1α pathways in Syntenin-1 arthritic mice and their obstruction in SDC-1 deficient animals. Consistently, dysregulation of SDC-1, mTOR, and HIF1α negated Syntenin-1 inflammatory phenotype in RA explants, while inhibition of HIF1α impaired synovial angiogenic imprint amplified by Syntenin-1. In conclusion, since the current therapies are ineffective on Syntenin-1 and SDC-1 expression in RA synovial tissue and blood, targeting this pathway and its interconnected metabolic intermediates may provide a novel therapeutic strategy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.