ReviewSeminars in immunopathology2017
Cellular and molecular pathways of structural damage in rheumatoid arthritis.
Review in Seminars in immunopathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
46 citing papers in PubMed.
- The Impact of NEAT1 on Inflammatory Responses and Processes in Arthropathic Diseases: Latest Findings and Perspectives.Biochemical genetics · 2026Review
- Pharmacogenetic biomarkers for predicting therapeutic response to JAK inhibitors in rheumatoid arthritis.Advances in laboratory medicine · 2026Article
- Spatiotemporally targeted nanocapsules combined with mild photothermal therapy regulate the synovial microenvironment in rheumatoid arthritis.Bioactive materials · 2026Article
- Targeting rheumatoid arthritis: a molecular perspective on biologic therapies and clinical progress.Journal of biological engineering · 2025Review
- Photobiomodulation control the expression of MMP, TNF-α and NK-1 receptors, improving allodynia and cartilage resistance in rheumatoid arthritis model.Lasers in medical science · 2025Article
- Article
- The relationship between the composite dietary antioxidant index and rheumatoid arthritis risk in American adults: the mediating role of BMI.Frontiers in immunology · 2025Article
- The role of anti-citrullinated protein antibody in pathogenesis of RA.Clinical and experimental medicine · 2024Review
- Fibroblast-like synoviocytes-derived exosomal circFTO deteriorates rheumatoid arthritis by enhancing N6-methyladenosine modification of SOX9 in chondrocytes.Arthritis research & therapy · 2024Article
- Toll-like receptor-2 induced inflammation causes local bone formation and activates canonical Wnt signaling.Frontiers in immunology · 2024Article
- Review
- The application and prospects of 3D printable microgel in biomedical science and engineering.International journal of bioprinting · 2023Review
- Comparison of the inhibitory effect of tocilizumab and etanercept on the progression of joint erosion in rheumatoid arthritis treatment.Scientific reports · 2022Article
- Update on the role of extracellular vesicles in rheumatoid arthritis.Expert reviews in molecular medicine · 2022Review
- The bone-protective mechanisms of active components from TCM drugs in rheumatoid arthritis treatment.Frontiers in pharmacology · 2022Review
- Traditional Tibetan medicine: therapeutic potential in rheumatoid arthritis.Frontiers in pharmacology · 2022Review
- ST3GAL3 Promotes the Inflammatory Response of Fibroblast-Like Synoviocytes in Rheumatoid Arthritis by Activating the TLR9/MyD88 Pathway.Mediators of inflammation · 2022Article
- The effect of long non-coding RNAs in joint destruction of rheumatoid arthritis.Frontiers in cell and developmental biology · 2022Review
- sTNFRII-Fc modification protects human UC-MSCs against apoptosis/autophagy induced by TNF-α and enhances their efficacy in alleviating inflammatory arthritis.Stem cell research & therapy · 2021Article
- Effect of Micro-/Nanoparticle Hybrid Hydrogel Platform on the Treatment of Articular Cartilage-Related Diseases.Gels (Basel, Switzerland) · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Structural damage of cartilage and bone tissue is a hallmark of rheumatoid arthritis (RA). The resulting joint destruction constitutes one of the major disease consequences for patients and creates a significant burden for the society. The main cells executing bone and cartilage degradation are osteoclasts and fibroblast-like synoviocytes, respectively. The function of both cell types is heavily influenced by the immune system. In the last decades, research has identified several mediators of structural damage, ranging from infiltrating immune cells and inflammatory cytokines to autoantibodies. These factors result in an inflammatory milieu in the affected joints which leads to an increased development and function of osteoclasts and the transformation of fibroblast-like synoviocytes towards a highly migratory and destructive phenotype. In addition, repair mechanisms mediated by osteoblasts and chondrocytes are strongly impaired by the presence of pro-inflammatory cytokines. This article will review the current knowledge on the mechanisms of joint inflammation and the destruction of bone and cartilage.
Indexed as
Identifiers
28597065What OpenQuestion holds
Registered trials
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.