ArticleArthritis & rheumatology (Hoboken, N.J.)2021
Lipopolysaccharide Binding Protein and CD14, Cofactors of Toll-like Receptors, Are Essential for Low-Grade Inflammation-Induced Exacerbation of Cartilage Damage in Mouse Models of Posttraumatic Osteoarthritis.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Association of low-grade inflammation caused by gut microbiota disturbances with osteoarthritis: A systematic review.Frontiers in veterinary science · 2022Pooled it
- Pathological mechanisms of osteoarthritis in the network of geriatric comorbidities: Emerging insights from organs-crosstalk.Journal of orthopaedic translation · 2026Review
- Presurgical immune biomarkers associated with pain intensity and pain interference recovery after total knee arthroplasty: findings from the PRIME-KNEE study.medRxiv : the preprint server for health sciences · 2026Article
- Efficacy and potential toxicity of Duhuo Qinjiao Decoction in osteoarthritis via the NF-κB pathway.Clinical rheumatology · 2026Article
- Gut microbiota dysbiosis and joint diseases: advances in the gut-joint axis.Frontiers in immunology · 2026Review
- Mechanistic insights into gut microbiota dysbiosis in osteoarthritis based on the gut-joint axis.Frontiers in immunology · 2026Review
- Combination of High-Fat Diet and Chronic Unpredictable Stress Synergistically Induces Osteoarthritis-Like Changes in Temporomandibular Joints in Rats.Mediators of inflammation · 2026Article
- Pig meniscus single-cell sequencing reveals highly active red zone chondrocyte populations involved in stemness maintenance and vascularization development.Journal of Zhejiang University. Science. B · 2025Article
- Loosening the Lid on Shoulder Osteoarthritis: How the Transcriptome and Metabolic Syndrome Correlate with End-Stage Disease.International journal of molecular sciences · 2025Article
- Exploring the Link Between Infections and Primary Osteoarthritis: A Next-Generation Metagenomic Sequencing Approach.International journal of molecular sciences · 2024Article
- TLR2 promotes traumatic deep venous thrombosis of the lower extremity following femoral fracture by activating the NF‑κB/COX‑2 signaling pathway in rats.Experimental and therapeutic medicine · 2024Article
- Hepatokines: unveiling the molecular and cellular mechanisms connecting hepatic tissue to insulin resistance and inflammation.Acta diabetologica · 2024Review
- Zwitterion-Lubricated Hydrogel Microspheres Encapsulated with Metformin Ameliorate Age-Associated Osteoarthritis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Mechanism of miR-7 mediating TLR4/TRAF6/NF-κB inflammatory pathway in colorectal cancer.Functional & integrative genomics · 2024Article
- Association of lipid-lowering drugs with osteoarthritis outcomes from a drug-target Mendelian randomization study.PloS one · 2024Article
- Prokineticin 2 is a catabolic regulator of osteoarthritic cartilage destruction in mouse.Arthritis research & therapy · 2023Article
- Imaging mass cytometry reveals tissue-specific cellular immune phenotypes in the mouse knee following ACL injury.Osteoarthritis and cartilage open · 2023Article
- Identification of EGFR as an essential regulator in chondrocytes ferroptosis of osteoarthritis using bioinformatics,Heliyon · 2023Article
- NOS inhibition reverses TLR2-induced chondrocyte dysfunction and attenuates age-related osteoarthritis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The Triterpenoid Nrf2 Activator, CDDO-Me, Decreases Neutrophil Senescence in a Murine Model of Joint Damage.International journal of molecular sciences · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveOsteoarthritis (OA) is initiated by pathogenic factors produced by multiple stimuli, including mechanical stress, metabolic stress, and/or inflammaging. This study was undertaken to identify novel low-grade inflammation-associated pathogenic mediators of OA.
methodsCandidate pathogenic molecules were screened using microarray data obtained from chondrocytes exposed to OA-associated catabolic factors. In mice with OA generated by destabilization of the medial meniscus (DMM), low-grade inflammation was induced by a high-fat diet or endotoxemia. Functions of candidate molecules in OA pathogenesis were examined using primary-culture chondrocytes from mice with DMM-induced OA, following intraarticular injection of adenovirus expressing the candidate gene. Specific functions of candidate genes were evaluated using whole-body gene-knockout mice.
resultsBioinformatics analysis identified multiple candidate pathogenic factors that were associated with low-grade inflammation, including components of the Toll-like receptor (TLR) signaling pathways (e.g., TLR-2, TLR-4, lipopolysaccharide binding protein [LBP], and CD14). Overexpression of the individual TLR signaling components in mouse joint tissue did not alter cartilage homeostasis. However, the low-grade inflammation induced by a high-fat diet or endotoxemia markedly enhanced posttraumatic OA cartilage destruction in mice, and this exacerbation of cartilage destruction was significantly abrogated in LBP
conclusionLBP and CD14, which are accessory molecules of TLRs, are necessary for the exacerbation of posttraumatic OA cartilage destruction resulting from low-grade inflammation, such as that triggered by a high-fat diet or endotoxemia.
Indexed as
Identifiers
What 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.