粒体自噬
自噬
破骨细胞
骨细胞
骨吸收
死孢子体1
PI3K/AKT/mTOR通路
成骨细胞
骨重建
品脱1
帕金
癌症研究
生物
细胞生物学
医学
内分泌学
信号转导
内科学
生物化学
受体
疾病
体外
帕金森病
细胞凋亡
作者
Shuai Wang,Zhantao Deng,Yuanchen Ma,Jiewen Jin,Fangjie Qi,Shuxian Li,Chang Liu,Feng‐Juan Lyu,Qiujian Zheng
摘要
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.
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