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- W3100923976 abstract "Significance Osteoarthritis (OA) is the most prevalent joint disease and has reached epidemic proportions in the United States. Currently, there are no effective therapeutic approaches to treat OA. Thus, there is an urgent need to develop mechanistically-based therapeutic strategies to treat this disease. In this study, we identified FoxO1 as a crucial mediator of the TGF-β pathway. We also showed that loss of FoxO1 in articular cartilage leads to OA-like pathologies and gain of FoxO1 in cartilage protects against surgically and loss-of-TGF-β-induced OA. Our study defines FoxO1 as a key downstream target of TGF-β signaling and the requisite role in the maintenance of postnatal articular cartilage homeostasis and implicates modulation of FoxO1 levels/activity as a potential therapeutic strategy for OA." @default.
- W3100923976 created "2020-11-23" @default.
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- W3100923976 date "2020-11-16" @default.
- W3100923976 modified "2023-10-14" @default.
- W3100923976 title "FoxO1 is a crucial mediator of TGF-β/TAK1 signaling and protects against osteoarthritis by maintaining articular cartilage homeostasis" @default.
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- W3100923976 doi "https://doi.org/10.1073/pnas.2017056117" @default.
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