ReviewMolecular and cellular biochemistry2017
Damage-associated molecular patterns in the pathogenesis of osteoarthritis: potentially novel therapeutic targets.
Review in Molecular and cellular biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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
68 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.
- Synovial inflammation and immune-stromal crosstalk in osteoarthritis-related synovial fibroblast research, 2006-2025: a bibliometric analysis.Frontiers in immunology · 2026Pooled it
- Ion-Enriched Solution Improves the Adhesion of Freshly Thawed Umbilical Cord-Derived Mesenchymal Stem Cells and Supports Cartilage Repair in a Rat Full-Thickness Cartilage Defect Model.Tissue engineering and regenerative medicine · 2026Article
- Article
- Metabolic disorders and osteoarthritis: novel insights into pathological mechanisms and therapeutic strategies.Life medicine · 2026Review
- A multiscale modeling approach to study the role of mechanics and inflammation in the pathophysiology of articular cartilage.Computers in biology and medicine · 2026Article
- Lung microbiota-derived deoxyinosine alleviates TBI-aggravated sepsis-induced lung injury via the S100A9/RAGE pathway.Journal of neuroinflammation · 2026Article
- Usability of Amorphous Manganese Oxide for Assessing the Proteoglycan Content in Articular Cartilage.Magnetic resonance in chemistry : MRC · 2026Article
- An etiopathogenesis of juvenile idiopathic arthritis: the protein-homeostasis-system hypothesis.Frontiers in pediatrics · 2026Review
- Integrating Mechanical Diagnosis and Therapy Within Multidisciplinary Biopsychosocial Care for Chronic Musculoskeletal Pain.Journal of orthopaedics and sports medicine · 2026Article
- Integrated Multiomics Analysis Identifies CDO1 as a Novel Therapeutic Target for OsteoarthritisEndocrine, metabolic & immune disorders drug targets · 2026Article
- CSF1-R inhibition attenuates posttraumatic osteoarthritis and quadriceps atrophy following ligament injury.The Journal of physiology · 2025Article
- A Multidimensional Definition of Pre-Osteoarthritis: Toward 21st-Century Subclinical Detection and Targeted Intervention.International journal of molecular sciences · 2025Review
- Mitochondria relay cholesterol signal exacerbates osteoarthritis in mice.Nature communications · 2025Article
- Exploring the mechanism of action of astragaloside in the treatment of osteoarthritis based on network pharmacology.Biomedical engineering online · 2025Article
- Joint Tissues: Convergence and Divergence of the Pathogenetic Mechanisms of Rheumatoid Arthritis and Osteoarthritis.International journal of molecular sciences · 2025Review
- Mechanobiochemical finite element model to analyze impact-loading-induced cell damage, subsequent proteoglycan loss, and anti-oxidative treatment effects in articular cartilage.Biomechanics and modeling in mechanobiology · 2025Article
- Construction of a glycolysis-related diagnostic model for osteoarthritis through integrated bioinformatics analysis and machine learning.Journal of orthopaedic surgery and research · 2025Article
- Chondrocyte lysates activate NLRP3 inflammasome-induced pyroptosis in synovial fibroblasts to exacerbate knee synovitis by downregulating caveolin-1.Arthritis research & therapy · 2025Article
- Functional Attributes of Synovial Fluid from Osteoarthritic Knee Exacerbate Cellular Inflammation and Metabolic Stress, and Fosters Monocyte to Macrophage Differentiation.Biomedicines · 2025Article
- The Mechanism by Which Estrogen Level Affects Knee Osteoarthritis Pain in Perimenopause and Non-Pharmacological Measures.International journal of molecular sciences · 2025Review
8 more citing papers are in PubMed but not listed here.
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 1 country.
Funding
Abstract
Osteoarthritis (OA) is a chronic disease that degrades the joints and is often associated with increasing age and obesity. The two most common sites of OA in adults are the knee and hip joints. Increased mechanical stress on the joint from obesity can cause the articular cartilage to degrade and release damage-associated molecular patterns (DAMPs). These DAMPs are involved in various molecular pathways that interact with nuclear factor-kappa B and result in the transcription of inflammatory cytokines and activation of matrix metalloproteinases that progressively destroy cartilage. This review focuses on the interactions and contribution to the pathogenesis and progression of OA through the DAMPs: high-mobility group box 1 (HMGB-1), the receptor for advanced glycation end-products (RAGE), the alarmin proteins S100A8 and S100A9, and heparan sulfate. HMGB-1 is released from damaged or necrotic cells and interacts with toll-like receptors (TLRs) and RAGE to induce inflammatory signals, as well as behave as an inflammatory cytokine to activate innate immune cells. RAGE interacts with HMGB-1, advanced glycation end-products, and innate immune cells to increase local inflammation. The alarmin proteins are released following cell damage and interact through TLRs to increase local inflammation and cartilage degradation. Heparan sulfate has been shown to facilitate the binding of HMGB-1 to RAGE and could play a role in the progression of OA. Targeting these DAMPs may be the potential therapeutic strategies for the treatment of OA.
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.