ArticleBioelectricity2022
Osteoarthritis: Mechanistic Insights, Senescence, and Novel Therapeutic Opportunities.
Article in Bioelectricity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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Who cites it
1 citing paper in PubMed.
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is the most common joint disease. In the last years, the research community has focused on understanding the molecular mechanisms that led to the pathogenesis of the disease, trying to identify different molecular and clinical phenotypes along with the discovery of new therapeutic opportunities. Different types of cell-to-cell communication mechanisms have been proposed to contribute to OA progression, including mechanisms mediated by connexin43 (Cx43) channels or by small extracellular vesicles. Furthermore, changes in the chondrocyte phenotype such as cellular senescence have been proposed as new contributors of the OA progression, changing the paradigm of the disease. The use of different drugs able to restore chondrocyte phenotype, to reduce cellular senescence and senescence-associated secretory phenotype components, and to modulate ion channel activity or Cx43 appears to be promising therapeutic strategies for the different types of OA. In this review, we aim to summarize the current knowledge in OA phenotypes related with aging and tissue damage and the new therapeutic opportunities currently available.
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Registered trials
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