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Autophagy: A Novel Therapeutic Target for Osteoporosis
Li Meng1,2,3, Zhongkai Zhang1,3,4,5, Yufeng Huang1,2,3
1Department of Pharmacology, School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, 250012 Shandong China.
None:
Autophagy is an evolutionarily conserved catabolic process in eukaryotes, which plays a vital role in the maintenance of cellular homeostasis. The occurrence of autophagy depends on lysosome, which is responsible for eliminating the dysfunctional cellular components, including misfolded proteins, impaired organelles and pathogens. Osteoporosis (OP) is a common bone metabolic disease, and it needs more therapeutic strategies that could restore the imbalance between bone formation and bone resorption, which is the main pathophysiological feature of OP. Interstingly, increasing evidence shows that autophagy is closely involved in bone metabolism, and its aberrant level leads to various skeletal system disorders, including OP. Autophagy regulates the survival, differentiation and function of bone marrow mesenchymal stromal cells (BMSCs), osteoblasts, osteocytes and osteoclasts, which are the major cell types in the bone microenvironment. Herein, we summarized the important advances of autophagy in bone metabolism, and the promising therapeutic strategies for OP by targeting autophagy. This review is aimed at providing novel insights for the prevention and treatment of OP via regulation of autophagy.
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