Int J Biol Sci 2020; 16(14):2675-2691. doi:10.7150/ijbs.46627

Review

The Role of Autophagy and Mitophagy in Bone Metabolic Disorders

Shuai Wang1,3#, Zhantao Deng1#, Yuanchen Ma1#, Jiewen Jin2, Fangjie Qi1,3, Shuxian Li1,3, Chang Liu3, Feng-Juan Lyu3✉, Qiujian Zheng1✉

1. Department of Orthopedics, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, 510080, China.
2. Department of Endocrinology, The First Affiliated Hospital of Sun Yat-sen University.
3. South China University of Technology-The University of Western Australia Joint Center for Regenerative Medicine Research, School of Medicine, South China University of Technology, Guangzhou, 510006, China.
#These authors contributed equally to this work.

This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.
Citation:
Wang S, Deng Z, Ma Y, Jin J, Qi F, Li S, Liu C, Lyu FJ, Zheng Q. The Role of Autophagy and Mitophagy in Bone Metabolic Disorders. Int J Biol Sci 2020; 16(14):2675-2691. doi:10.7150/ijbs.46627. Available from http://www.ijbs.com/v16p2675.htm

File import instruction

Abstract

Bone metabolic disorders include osteolysis, osteoporosis, osteoarthritis and rheumatoid arthritis. Osteoblasts and osteoclasts are two major types of cells in bone constituting homeostasis. The imbalance between bone formation by osteoblasts and bone resorption by osteoclasts has been shown to have a direct contribution to the onset of these diseases. Recent evidence indicates that autophagy and mitophagy, the selective autophagy of mitochondria, may play a vital role in regulating the proliferation, differentiation and function of osteoblasts and osteoclasts. Several signaling pathways, including PINK1/Parkin, SIRT1, MAPK8/FOXO3, Beclin-1/BECN1, p62/SQSTM1, and mTOR pathways, have been implied in the regulation of autophagy and mitophagy in these cells. Here we review the current progress about the regulation of autophagy and mitophagy in osteoblasts and osteoclasts in these bone metabolic disorders, as well as the molecular signaling activated or deactivated during this process. Together, we hope to draw attention to the role of autophagy and mitophagy in bone metabolic disorders, and their potential as a new target for the treatment of bone metabolic diseases and the requirements of further mechanism studies.

Keywords: autophagy, mitophagy, bone metabolic disorder, osteoblast, osteoclast