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FGF1 reduces cartilage injury in osteoarthritis via regulating AMPK/Nrf2 pathway

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Abstract

Osteoarthritis (OA) is a systemic joint degenerative disease involving a variety of cytokines and growth factors. In this study, we investigated the protective effect of fibroblast growth factor 1 (FGF1) knockdown on OA and its underlying mechanisms in vitro. In addition, we evaluated the effect of FGF1 knockout on the destabilization of the medial meniscus (DMM) and examined the anterior and posterior cruciate ligament model in vivo. FGF1 affects OA cartilage destruction by increasing the protein expression of Nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1), which is associated with the phosphorylation of AMPK and its substrates. Our study showed that FGF1 knockdown could reverse the oxidative damage associated with osteoarthritis. Nrf2 knockdown eliminated the antioxidant effect of FGF1 knockdown on chondrocytes. Furthermore, AMPK knockdown could stop the impact of FGF1 knockdown on osteoarthritis. These findings suggested that FGF1 knockdown could effectively prevent and reverse osteoarthritis by activating AMPK and Nrf2 in articular chondrocytes.

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The corresponding author’s data supporting this study’s funding are available upon reasonable request.

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Authors

Contributions

LY-X and ZG conceived and designed the study, and acquired data. All authors contributed to data analysis and manuscript preparation. All authors read and approved the final manuscript. All the authors read and approved the final manuscript and agree to be accountable for all aspects of the work.

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Correspondence to Gang Zhao.

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The authors declare that they have no competing interests.

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All procedures related to the use and care of animals in this study were approved by the ethics committee of Kunming Medical University approved our animal experiment procedure (KMUWECA 20210007).

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Li, YX., Shu, J., Kou, Nn. et al. FGF1 reduces cartilage injury in osteoarthritis via regulating AMPK/Nrf2 pathway. J Mol Histol 54, 427–438 (2023). https://doi.org/10.1007/s10735-023-10143-8

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  • DOI: https://doi.org/10.1007/s10735-023-10143-8

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