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Autophagy as a target for glucocorticoid-induced osteoporosis therapy

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Abstract

Autophagy takes part in regulating the eukaryotic cells function and the progression of numerous diseases, but its clinical utility has not been fully developed yet. Recently, mounting evidences highlight an important correlation between autophagy and bone homeostasis, mediated by osteoclasts, osteocytes, bone marrow mesenchymal stem cells, and osteoblasts, and autophagy plays a vital role in the pathogenesis of glucocorticoid-induced osteoporosis (GIOP). The combinations of autophagy activators/inhibitors with anti-GIOP first-line drugs or some new autophagy-based manipulators, such as regulation of B cell lymphoma 2 family proteins and caspase-dependent clearance of autophagy-related gene proteins, are likely to be the promising approaches for GIOP clinical treatments. In view of the important role of autophagy in the pathogenesis of GIOP, here we review the potential mechanisms about the impacts of autophagy in GIOP and its association with GIOP therapy.

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Acknowledgements

This study was jointly funded by the Natural Science Foundation of China (nos. 81503591, 81774338, 81674000), Science and Technology Projects of Guangdong Province (nos. 2014A020221021, 2016A020226006), Natural Science Foundation of Guangdong Province (no. 2014A030310082), Excellent Doctor Project of the First School of Clinic Medicine of Guangzhou University of Chinese Medicine (nos. YB201602, YB201501).

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Correspondence to Xiaobing Jiang.

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Shen, G., Ren, H., Shang, Q. et al. Autophagy as a target for glucocorticoid-induced osteoporosis therapy. Cell. Mol. Life Sci. 75, 2683–2693 (2018). https://doi.org/10.1007/s00018-018-2776-1

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  • DOI: https://doi.org/10.1007/s00018-018-2776-1

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