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P53: A Key Target in the Development of Osteoarthritis

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Abstract

Osteoarthritis (OA), a chronic degenerative disease characterized mainly by damage to the articular cartilage, is increasingly relevant to the pathological processes of senescence, apoptosis, autophagy, proliferation, and differentiation of chondrocytes. Clinical strategies for osteoarthritis can only improve symptoms and even along with side effects due to age, sex, disease, and other factors. Therefore, there is an urgent need to identify new ideas and targets for current clinical treatment. The tumor suppressor gene p53, which has been identified as a potential target for tumor therapeutic intervention, is responsible for the direct induction of the pathological processes involved in OA modulation. Consequently, deciphering the characteristics of p53 in chondrocytes is essential for investigating OA pathogenesis due to p53 regulation in an array of signaling pathways. This review highlights the effects of p53 on senescence, apoptosis, and autophagy of chondrocytes and its role in the development of OA. It also elucidates the underlying mechanism of p53 regulation in OA, which may help provide a novel strategies for the clinical treatment of OA.

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Funding

The authors gratefully acknowledge the financial support from the National Natural Sciences Foundation of China (Grant No. 81800386), Hunan Provincial Natural Science Foundation of China (2021JJ30020), and Scientific Research Project of Health Commission of Hunan Province (20201907, 202101021784).

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Ma, W., Tan, X., Xie, Z. et al. P53: A Key Target in the Development of Osteoarthritis. Mol Biotechnol 66, 1–10 (2024). https://doi.org/10.1007/s12033-023-00736-9

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