ReviewAnnals of the New York Academy of Sciences2011
Mechanotransduction and cartilage integrity.
Review in Annals of the New York Academy of Sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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
50 citing papers in PubMed, 103 citations in OpenAlex.
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- Membrane Ruffles: Composition, Function, Formation and Visualization.International journal of molecular sciences · 2024Review
- Hippo-PKCζ-NFκB signaling axis: A druggable modulator of chondrocyte responses to mechanical stress.iScience · 2024Article
- Biomechanics of the Human Osteochondral Unit: A Systematic Review.Materials (Basel, Switzerland) · 2024Review
- Role of mechanically-sensitive cation channels Piezo1 and TRPV4 in trabecular meshwork cell mechanotransduction.Human cell · 2024Review
- Unraveling cartilage degeneration through synergistic effects of hydrostatic pressure and biomimetic temperature increase.iScience · 2023Article
- A Review of the Role of Bioreactors for iPSCs-Based Tissue-Engineered Articular Cartilage.Tissue engineering and regenerative medicine · 2023Review
- Tendon-regulating and bone-setting manipulation promotes the recovery of synovial inflammation in rabbits with knee osteoarthritis via the TLR4-MyD88-NF-κB signaling pathway.Annals of translational medicine · 2023Article
- The intricate mechanism of PLS3 in bone homeostasis and disease.Frontiers in endocrinology · 2023Review
- Fenoldopam Sensitizes Primary Cilia-Mediated Mechanosensing to Promote Osteogenic Intercellular Signaling and Whole Bone Adaptation.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Article
- State of Knowledge on Molecular Adaptations to Exercise in Humans: Historical Perspectives and Future Directions.Comprehensive Physiology · 2022Article
- Location-Dependent Human Osteoarthritis Cartilage Response to Realistic Cyclic Loading:Frontiers in bioengineering and biotechnology · 2022Article
- The Role of Mechanically-Activated Ion Channels Piezo1, Piezo2, and TRPV4 in Chondrocyte Mechanotransduction and Mechano-Therapeutics for Osteoarthritis.Frontiers in cell and developmental biology · 2022Review
- Integrins, cadherins and channels in cartilage mechanotransduction: perspectives for future regeneration strategies.Expert reviews in molecular medicine · 2021Review
- Mechanotransducive Biomimetic Systems for Chondrogenic Differentiation In Vitro.International journal of molecular sciences · 2021Review
- Plastin 3 in health and disease: a matter of balance.Cellular and molecular life sciences : CMLS · 2021Review
- Talar OsteoPeriostic grafting from the Iliac Crest (TOPIC) for large medial talar osteochondral defects : Operative technique.Operative Orthopadie und Traumatologie · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Osteoarthritis (OA) is characterized by the breakdown of articular cartilage that is mediated in part by increased production of matrix metalloproteinases (MMPs) and aggrecanases (ADAMTS), enzymes that degrade components of the cartilage extracellular matrix. Efforts to design synthetic inhibitors of MMPs/ADAMTS have only led to limited clinical success. In addition to pharmacologic therapies, physiologic joint loading is widely recommended as a nonpharmacologic approach to improve joint function in osteoarthritis. Clinical trials report that moderate levels of exercise exert beneficial effects, such as improvements in pain and physical function. Experimental studies demonstrate that mechanical loading mitigates joint destruction through the downregulation of MMPs/ADAMTS. However, the molecular mechanisms underlying these effects of physiologic loading on arthritic joints are not well understood. We review here the recent progress on mechanotransduction in articular joints, highlighting the mediators and pathways in the maintenance of cartilage integrity, especially in the prevention of cartilage degradation in OA.
Indexed as
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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.