ArticleBlood2015
Transglutaminase factor XIII promotes arthritis through mechanisms linked to inflammation and bone erosion.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
33 citing papers in PubMed, 47 citations in OpenAlex.
- Activation of the Coagulation Cascade as a Universal Danger Sign.Current issues in molecular biology · 2025Review
- Meniscus gene expression profiling of inner and outer zone meniscus tissue compared to cartilage and passaged monolayer meniscus cells.Scientific reports · 2024Article
- Article
- Fungal transglutaminase domain-containing proteins are involved in hyphal protection at the septal pore against wounding.Molecular biology of the cell · 2023Article
- Multi-Omic Temporal Landscape of Plasma and Synovial Fluid-Derived Extracellular Vesicles Using an Experimental Model of Equine Osteoarthritis.International journal of molecular sciences · 2023Article
- Article
- Expression of factor XIII originating from synovial fibroblasts and macrophages induced by interleukin-6 signaling.Inflammation and regeneration · 2023Article
- TGFβ1-Induced Transglutaminase-2 Triggers Catabolic Response in Osteoarthritic Chondrocytes by Modulating MMP-13.Tissue engineering and regenerative medicine · 2021Article
- Article
- Factor XIII-A in Diseases: Role Beyond Blood Coagulation.International journal of molecular sciences · 2021Review
- Article
- Transglutaminases and Obesity in Humans: Association ofInternational journal of molecular sciences · 2020Article
- Osteoclast Multinucleation: Review of Current Literature.International journal of molecular sciences · 2020Review
- Non-invasive in vivo imaging of acute thrombosis: development of a novel factor XIIIa radiotracer.European heart journal. Cardiovascular Imaging · 2020Article
- Plasminogen activation in the musculoskeletal acute phase response: Injury, repair, and disease.Research and practice in thrombosis and haemostasis · 2020Review
- Proteolytic and nonproteolytic activation mechanisms result in conformationally and functionally different forms of coagulation factor XIII A.The FEBS journal · 2020Article
- Tocilizumab Effects on Coagulation Factor XIII in Patients with Rheumatoid Arthritis.Advances in therapy · 2019Article
- Review
- Transglutaminases in Monocytes and Macrophages.Medical sciences (Basel, Switzerland) · 2018Review
- Coagulopathies and inflammatory diseases: '…glimpse of a Snark'.Current opinion in immunology · 2018Review
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Rheumatoid arthritis is a chronic inflammatory disease characterized by synovial hyperplasia, inflammatory cell infiltration, irreversible cartilage and bone destruction, and exuberant coagulation system activity within joint tissue. Here, we demonstrate that the coagulation transglutaminase, factor XIII (fXIII), drives arthritis pathogenesis by promoting local inflammatory and tissue degradative and remodeling events. All pathological features of collagen-induced arthritis (CIA) were significantly reduced in fXIII-deficient mice. However, the most striking difference in outcome was the preservation of cartilage and bone in fXIIIA(-/-) mice concurrent with reduced osteoclast numbers and activity. The local expression of osteoclast effectors receptor activator of nuclear factor-κB ligand (RANKL) and tartrate resistant acid phosphatase were significantly diminished in CIA-challenged and even unchallenged fXIIIA(-/-) mice relative to wild-type animals, but were similar in wild-type and fibrinogen-deficient mice. Impaired osteoclast formation in fXIIIA(-/-) mice was not due to an inherent deficiency of monocyte precursors, but it was linked to reduced RANKL-driven osteoclast formation. Furthermore, treatment of mice with the pan-transglutaminase inhibitor cystamine resulted in significantly diminished CIA pathology and local markers of osteoclastogenesis. Thus, eliminating fXIIIA limits inflammatory arthritis and protects from cartilage and bone destruction in part through mechanisms linked to reduced RANKL-mediated osteoclastogenesis. In summary, therapeutic strategies targeting fXIII activity may prove beneficial in limiting arthropathies and other degenerative bone diseases.
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