ReviewFASEB journal : official publication of the Federation of American Societies for Experimental Biology2013
Fluid shear stress-induced osteoarthritis: roles of cyclooxygenase-2 and its metabolic products in inducing the expression of proinflammatory cytokines and matrix metalloproteinases.
Review in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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
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Who cites it
42 citing papers in PubMed, 82 citations in OpenAlex.
- Metabolic reprogramming in polyol pathway contributes to anti-inflammatory effect of glucosamine salts on synovial fibroblasts.npj metabolic health and disease · 2026Article
- Ultrashort echo time bi-component analysis of tibiotalar articular cartilage after long-distance running.European radiology · 2026Article
- Blockade of the Notch Pathway by Inhibition of Fucosylation Ameliorates Chondrocyte Inflammation and Extracellular Matrix Degradation.Journal of inflammation research · 2025Article
- Low fluid shear stress promotes chondrocyte proliferation and extracellular matrix secretion by downregulating mir-143-3p and activating the ERK5/KLF4 signaling pathway.Scientific reports · 2024Article
- Low shear stress protects chondrocytes from IL-1β-induced apoptosis by activating ERK5/KLF4 signaling and negatively regulating miR-143-3p.Journal of orthopaedic surgery and research · 2024Article
- Review
- Potential Therapeutic Mechanism of Radix Angelicae Biseratae and Dipsaci Radix Herb Pair against Osteoarthritis: Based on Network Pharmacology and Molecular Docking.Evidence-based complementary and alternative medicine : eCAM · 2023Article
- Loganin attenuates interleukin-1The Journal of international medical research · 2022Article
- Knee Pain from Osteoarthritis: Pathogenesis, Risk Factors, and Recent Evidence on Physical Therapy Interventions.Journal of clinical medicine · 2022Review
- Elevation of α-1,3 fucosylation promotes the binding ability of TNFR1 to TNF-α and contributes to osteoarthritic cartilage destruction and apoptosis.Arthritis research & therapy · 2022Article
- Rho GTPase signaling in rheumatic diseases.iScience · 2022Review
- Effects of mechanical stimulation on metabolomic profiles of SW1353 chondrocytes: shear and compression.Biology open · 2022Article
- High-Molecular-Weight Hyaluronic Acid Inhibits IL-1β-Induced Synovial Inflammation and Macrophage Polarization through the GRP78-NF-κB Signaling Pathway.International journal of molecular sciences · 2021Article
- Recent Advances in Understanding the Role of Cartilage Lubrication in Osteoarthritis.Molecules (Basel, Switzerland) · 2021Review
- Biofilm formation in periprosthetic joint infections.Annals of joint · 2021Article
- Inhibitory Effects of IL-6-Mediated Matrix Metalloproteinase-3 and -13 byPharmaceuticals (Basel, Switzerland) · 2021Article
- A Roadmap of In Vitro Models in Osteoarthritis: A Focus on Their Biological Relevance in Regenerative Medicine.Journal of clinical medicine · 2021Review
- Aberrant Fluid Shear Stress Contributes to Articular Cartilage Pathogenesis via Epigenetic Regulation of ZBTB20 by H3K4me3.Journal of inflammation research · 2021Article
- Mitochondria in Injury, Inflammation and Disease of Articular Skeletal Joints.Frontiers in immunology · 2021Review
- Less mechanical loading attenuates osteoarthritis by reducing cartilage degeneration, subchondral bone remodelling, secondary inflammation, and activation of NLRP3 inflammasome.Bone & joint research · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The mechanical overloading of cartilage is involved in the pathophysiology of osteoarthritis (OA) by both biochemical and mechanical pathways. The application of fluid shear stress to chondrocytes recapitulates the earmarks of OA, as evidenced by the release of proinflammatory cytokines (PICs), matrix metalloproteinases (MMPs), and apoptotic factors. Dysregulations or mutations in these genes might directly cause OA in addition to determining the stage at which OA becomes apparent, the joint sites involved, and the severity of the disease and how rapidly it progresses. However, the underlying mechanisms remain unknown. In this review, we propose that the dysregulation of cyclooxygenase-2 (COX-2) is associated with fluid shear stress-induced OA via its metabolic products at different stages of the disease. Indeed, high fluid shear stress rapidly induces the production of PICs and MMPs via COX-2-derived prostaglandin (PG)E2 at the early stage of OA. In contrast, prolonged shear exposure (>12 h) aggravates the condition by concurrently up-regulating the expression of proapoptotic genes and down-regulating the expression of antiapoptotic genes in a 15-deoxy-Δ (12,14)-prostaglandin J2 (15d-PGJ2)-dependent manner at the late stage of disease. These observations may help to resolve long-standing questions in OA progression and provide insight for development of strategies to treat and combat OA.
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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.