ArticleBone & joint research2022
The role of AGEs in pathogenesis of cartilage destruction in osteoarthritis.
Article in Bone & joint research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.
What it found
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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.
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
17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 25 citations in OpenAlex.
- Metformin for knee osteoarthritis in overweight and obese adults: a systematic review and meta-analysis of efficacy, safety, and disease-modifying anti-inflammatory potential.Inflammopharmacology · 2026Pooled it
- Mechanisms of active metabolites from traditional Chinese medicine in osteoarthritis: a critical review.Frontiers in pharmacology · 2026Pooled it
- Oxygen tension alters cartilage redox balance in response to traumatic impact.Bone & joint research · 2026Article
- Article
- Dysregulation of the glycolysis-mitochondrial metabolism axis in osteoarthritis: mechanisms and therapeutic implications.Journal of orthopaedic translation · 2026Review
- Longitudinal multicohort evidence for bidirectional diabetes arthritis links in older adults.iScience · 2026Article
- PBA-enriched glycated/ glycosylated synovial fluid proteomic signatures associated with metabolic dysregulation and cartilage degeneration in osteoarthritis with type 2 diabetes.Journal of translational medicine · 2026Article
- Integrative multi-omics analysis reveals gut microbiota-derived metabolites and immune regulatory pathways in osteoarthritis pathogenesis.Journal of orthopaedic surgery and research · 2026Article
- Diabetes-Related Metabolic Osteoarthritis: Advanced Glycation-Collagen Axis, Cartilage Stiffening, and Biomaterials-Based Therapeutic Strategies.International journal of nanomedicine · 2026Review
- Cytosolic phospholipase A2 as a therapeutic target for degenerative joint diseases.Bone research · 2025Article
- Serum Levels of HMGB1, hS100A8/A9, and sRAGE in Patients with Knee and Hip Osteoarthritis: Inflammatory Biomarkers of Disease Activity.Journal of clinical medicine · 2025Article
- Integrated bioinformatics and network pharmacology to identify and validate macrophage polarization related hub genes in the treatment of osteoarthritis with Astragalus membranaceus.Journal of orthopaedic surgery and research · 2025Article
- Changes in Gene Expression Patterns in Young and Senescent Fibroblasts in Glycated Three-Dimensional Collagen Matrices.International journal of molecular sciences · 2025Article
- Metabolic-BMI phenotypes as nutritional risk indicators for osteoarthritis: evidence from a prospective cohort of UK adults.Frontiers in nutrition · 2025Article
- Exploring the mechanism of action ofHeliyon · 2024Article
- Autophagy in Osteoarthritis: A Double-Edged Sword in Cartilage Aging and Mechanical Stress Response: A Systematic Review.Journal of clinical medicine · 2024Review
- Sugar-coated bullets: Unveiling the enigmatic mystery 'sweet arsenal' in osteoarthritis.Heliyon · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is a degenerative disease resulting from progressive joint destruction caused by many factors. Its pathogenesis is complex and has not been elucidated to date. Advanced glycation end products (AGEs) are a series of irreversible and stable macromolecular complexes formed by reducing sugar with protein, lipid, and nucleic acid through a non-enzymatic glycosylation reaction (Maillard reaction). They are an important indicator of the degree of ageing. Currently, it is considered that AGEs accumulation in vivo is a molecular basis of age-induced OA, and AGEs production and accumulation in vivo is one of the important reasons for the induction and acceleration of the pathological changes of OA. In recent years, it has been found that AGEs are involved in a variety of pathological processes of OA, including extracellular matrix degradation, chondrocyte apoptosis, and autophagy. Clearly, AGEs play an important role in regulating the expression of OA-related genes and maintaining the chondrocyte phenotype and the stability of the intra-articular environment. This article reviews the latest research results of AGEs in a variety of pathological processes of OA, to provide a new direction for the study of OA pathogenesis and a new target for prevention and treatment. Cite this article:
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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 Socratic graph.