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| Autor principal: | |
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| Format: | Recurso digital |
| Idioma: | anglès |
| Publicat: |
Zenodo
2024
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| Matèries: | |
| Accés en línia: | https://doi.org/10.5281/zenodo.13835778 |
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- <p>Osteoarthritis (OA) is a major cause of chronic pain and joint damage, involving low-grade synovitis that contributes to disease progression. Fibroblast-like synoviocytes (FLSs) are central to this process, producing inflammatory cytokines regulated by calcium (Ca2+) signaling. Targeting Ca2+ signaling through store-operated calcium entry (SOCE) could help reduce inflammation in OA.We tested two novel SOCE-negative modulators (CIC-39 and BIP-26) and two drugs (methotrexate and celecoxib) on inflamed OA-FLSs. CIC-39 and BIP-26 reduced Ca2+ influx without affecting cell morphology or viability. Methotrexate and the SOCE modulators showed trends toward reducing cytokine expression, though results were not statistically significant. Celecoxib induced cell death in a dose-dependent manner and caused cell cycle arrest. Overall, SOCE modulators show potential as a new treatment strategy for OA.</p>