ReviewInternational journal of experimental pathology2009
Analysing the role of endogenous matrix molecules in the development of osteoarthritis.
Review in International journal of experimental pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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
62 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.
- Pooled it
- Unicompartmental and bicompartmental knee osteoarthritis show different patterns of mononuclear cell infiltration and cytokine release in the affected joints.Clinical and experimental immunology · 2015Trial
- Protein modification by deamidation indicates variations in joint extracellular matrix turnover.The Journal of biological chemistry · 2012Trial
- CSPG4Osteoarthritis and cartilage open · 2026Article
- Article
- Integrative Single-Cell and Spatial Transcriptomics Identifies CRIP1Mediators of inflammation · 2026Article
- A Multidimensional Definition of Pre-Osteoarthritis: Toward 21st-Century Subclinical Detection and Targeted Intervention.International journal of molecular sciences · 2025Review
- Early diagnosis and targeted intervention based on the pathogenesis of rapidly progressive osteoarthritis of the hip.World journal of orthopedics · 2025Review
- Exploring the mechanism of action of astragaloside in the treatment of osteoarthritis based on network pharmacology.Biomedical engineering online · 2025Article
- Unraveling Osteoarthritis: Mechanistic Insights and Emerging Therapies Targeting Pain and Inflammation.Biomolecules · 2025Review
- Targeting TREM-1 receptors with metformin and pravastatin modulate monosodium iodoacetate-induced osteoarthritis.Inflammopharmacology · 2025Article
- Rethinking Osteoarthritis Management: Synergistic Effects of Chronoexercise, Circadian Rhythm, and Chondroprotective Agents.Biomedicines · 2025Article
- Autoantibodies cause nociceptive sensitization in a mouse model of degenerative osteoarthritis.Pain · 2024Article
- Low-Grade Inflammatory Mediators and Metalloproteinases Yield Synchronous and Delayed Responses to Mechanical Joint Loading.Cartilage · 2024Article
- Immune System-Related Plasma Pathogenic Extracellular Vesicle Subpopulations Predict Osteoarthritis Progression.International journal of molecular sciences · 2024Article
- Evaluation of the Role of Myofibroblast and Fibronectin in the Aetiopathogenesis of Cholesteatoma.Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India · 2024Article
- The joint protective function of live- and dead-Aging · 2024Article
- Integrin signalling in joint development, homeostasis and osteoarthritis.Nature reviews. Rheumatology · 2024Review
- Engineering approaches for RNA-based and cell-based osteoarthritis therapies.Nature reviews. Rheumatology · 2024Review
- Comprehensive characterization of pathogenic synovial fluid extracellular vesicles from knee osteoarthritis.Clinical immunology (Orlando, Fla.) · 2023Article
2 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
1 author at 1 institution in 1 country.
Funding
Abstract
Osteoarthritis (OA) is the most common form of arthritis worldwide. In this condition, damage to the extracellular matrix (ECM) of cartilage occurs, resulting in joint destruction. Factors mediating cartilage damage include mechanical injury, cytokine and superoxide release on a background of genetic susceptibility and obesity. Studies of arthritic cartilage show increased production of ECM molecules including type II collagen, cartilage oligomeric matrix protein, fibronectin (FN) and fibromodulin. Recent reports suggest that ECM proteins may become endogenous catabolic factors during joint damage. Activation of pro-inflammatory pathways by ECM proteins has led to their description as damage-associated molecular patterns (DAMPs). The ECM proteins involved include fibromodulin, which activates the complement pathway and may promote the persistence of joint inflammation. Fragmentation of type II collagen, FN and hyaluronan reveals cryptic epitopes that stimulate proteolytic enzymes including matrix metalloproteinases and aggrecanases (ADAMTSs - a disintegrin and metalloproteinase with thrombospondin type 1 motifs). Proteolytic fragments also stimulate the release of nitric oxide, chemokines and cytokines and activation of the MAP kinases. Reports are emerging that the receptors for the fragments described involve interaction with integrins and toll-like receptors. In this review the contribution of endogenous ECM molecules to joint destruction will be discussed. A deeper understanding of the pathways stimulated by endogenous ligands could offer potential avenues for novel therapies in the future.
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.