ReviewLife (Basel, Switzerland)2025
Breaking Down Osteoarthritis: Exploring Inflammatory and Mechanical Signaling Pathways.
Review in Life (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Coumarins in musculoskeletal health: a systematic review.Frontiers in nutrition · 2026Pooled it
- Small extracellular vesicles in osteoarthritis: A double‑edged sword regulating inflammation and cartilage homeostasis (Review).International journal of molecular medicine · 2026Review
- Redox-Regulating Propolis- and Honey-Containing Hydrogels in Osteoarthritis.Antioxidants (Basel, Switzerland) · 2026Review
- Article
- Multi-Tissue Crosstalk Regulating Meniscus Healing Under Inflammation and Physiological Loading.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Drug-tolerant persister cells use conserved adaptive transcriptional programs.Translational cancer research · 2026Article
- Review
- Ectoine Inhibits IL-1β-Induced Inflammation by Suppressing the NF-κB Pathway in Chondrocytes and Alleviates Osteoarthritis in a Rat Model.Biomedicines · 2026Article
- Optical Spectral Transmission Imaging in Patients with Osteoarthritis: A Comparative Study with Joint Ultrasound and Clinical Markers.Rheumatology and therapy · 2026Article
- The NLRP12 Osteoimmune Checkpoint: Coordinating Inflammatory Signaling and Bone Remodeling.Biomedicines · 2026Review
- Cryogel-based therapeutic platforms for disease modification in osteoarthritis.npj biomedical innovations · 2026Review
- Chondroprotective Effects of Enzyme-Treated Extract fromInternational journal of molecular sciences · 2026Article
- Abnormal Stress Reduced miR-330 Supplementation Alleviates Osteoarthritis Progression by Suppressing Osteochondral Catabolism.Aging cell · 2026Article
- Is multi-joint hip and knee osteoarthritis more than the sum of its parts?Osteoarthritis and cartilage open · 2026Article
- Targeting TLR4/non-canonical NF-κB pathway by Bushen Bitong recipe enhances BMSCs-based cartilage repair in osteoarthritis.Biochemistry and biophysics reports · 2026Article
- Article
- Cellular Products with Anti-Inflammatory Properties for the Treatment of Cartilage Lesions.International journal of molecular sciences · 2026Review
- Review
- TCF4 contributes to OA progression by regulating the transcription of LOXL1.Journal of inflammation (London, England) · 2026Article
- Serum Dkk-1 Is Associated with Pain Intensity, Flare-Ups, and Bone Mineral Density in Non-Obese Patients with Knee Osteoarthritis: A Single-Center, Cross-Sectional Study.International journal of molecular sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is a chronic progressive joint disease characterized by cartilage degradation, subchondral bone remodeling, and synovial inflammation. This complex disorder arises from the interplay between mechanical stress and inflammatory processes, which is mediated by interconnected molecular signaling pathways. This review explores the dual roles of inflammatory and mechanical signaling in OA pathogenesis, focusing on crucial pathways such as NF-kB, JAK/STAT, and MAPK in inflammation, as well as Wnt/β-catenin, Integrin-FAK, and Hippo-YAP/TAZ in mechanotransduction. The interplay between these pathways highlights a vicious cycle wherein mechanical stress exacerbates inflammation, and inflammation weakens cartilage, increasing its vulnerability to mechanical damage. Additionally, we discuss emerging therapeutic strategies targeting these pathways, including inhibitors of cartilage-degrading enzymes, anti-inflammatory biologics, cell-based regenerative approaches, and non-pharmacological mechanical interventions. By dissecting the molecular mechanisms underlying OA, this review aims to provide insights into novel interventions that address both inflammatory and mechanical components of the disease, paving the way for precision medicine in OA management.
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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.