ReviewBiomolecules2025
Unraveling Osteoarthritis: Mechanistic Insights and Emerging Therapies Targeting Pain and Inflammation.
Review in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed.
- Microfragmented Adipose Tissue in Pain Management: Bridging Regenerative Biology and Clinical Therapeutics.Pain and therapy · 2026Review
- Effects of Acupuncture at ST36 and SP6 on Activity Levels and Pain Thresholds Through Interleukin-1, Interleukin-6, Cortisol, and Matrix Metalloproteinase-13 Modulation in an Osteoarthritis Rat Model.Journal of pharmacopuncture · 2026Article
- Oxeiptosis-Associated Molecular Subtyping and Immune Microenvironment Heterogeneity in Osteoarthritis.Biomedicines · 2026Article
- Vestitol Ameliorates Ferroptosis-Associated Features and Osteoarthritis Progression Through Modulation of the GSK3B/Nrf2/GPX4 Pathway.Cell biochemistry and biophysics · 2026Article
- Comparative Histopathological Effects of Intra-Articular Bevacizumab, Ranibizumab, and Aflibercept in Experimental Osteoarthritis.Journal of clinical medicine · 2026Article
- Systemic implications of osteoarthritis: from local degeneration to systemic metabolic Dysregulation.Journal of translational medicine · 2026Review
- Cellular Products with Anti-Inflammatory Properties for the Treatment of Cartilage Lesions.International journal of molecular sciences · 2026Review
- Synovial Fluid Characteristics and Pain Recovery Trajectory Following Rehabilitation in Patients with Meniscal Tears: A Retrospective Cohort Study.Healthcare (Basel, Switzerland) · 2026Article
- Developmentally Inspired, Mechanical-Metabolic Dual Gradient Osteochondral Constructs Bridging Regeneration and Therapeutic Screening.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- TCF4 contributes to OA progression by regulating the transcription of LOXL1.Journal of inflammation (London, England) · 2026Article
- [The role and mechanism of chemokine network in promoting osteoarthritis progression by regulating synovial macrophage heterogeneity].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2026Review
- Extracellular matrix remodeling in the pathogenesis and therapeutic strategies of rheumatoid arthritis.Clinical and experimental medicine · 2026Review
- Integrative multi-omics identifiesFrontiers in immunology · 2026Article
- Integrating Mechanical Loading, Mechanotransduction, and Biological Responses in Musculoskeletal Tissues Across the Lifespan: Regulation Influenced by Cells, Extracellular Matrix, and Sex.Results and problems in cell differentiation · 2026Review
- Article
- 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
- Mechanisms of synovial macrophage polarization in osteoarthritis pathogenesis and their therapeutic implications.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Osteoarthritis (OA) is now widely recognized not merely as a cartilage-centric disease but as a multifactorial disorder affecting the entire joint as an organ, including the articular cartilage, subchondral bone, synovium, ligaments, menisci, and the innervating neural elements. This review explores the complex pathophysiology of OA with a focus on the emerging mechanisms of pain and inflammation that extend beyond articular cartilage degradation. Joint inflammation driven by immune activation in response to cellular stress signals promotes the release of pro-inflammatory mediators and catabolic enzymes. Key signaling pathways such as NF-κB, MAPKs, and JAK/STAT amplify these responses, and pain is sustained through peripheral and central sensitization, contributing to exacerbating symptoms even in the absence of visible joint damage. This review also integrates molecular and cellular mechanisms to highlight innovative therapies aimed at modifying both the structural damage and neurosensory drivers of pain. These approaches offer the potential to not only alleviate symptoms but also alter disease progression, signaling a move toward personalized, mechanism-based treatments. Given the intricate interactions among joint tissues, immune activation, and sensory processing, a comprehensive strategy that targets both structural degeneration and neuroinflammation is essential for the future of OA management. Emphasizing the joint as an integrated organ, we advocate for translational research linking molecular pathology with clinically meaningful outcomes.
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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 OpenQuestion graph.