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自噬在破骨细胞分化和骨吸收功能中的作用。

The Role of Autophagy in Osteoclast Differentiation and Bone Resorption Function.

机构信息

Department of Anatomy, Histology, Forensic Medicine and Orthopaedics, Unit of Histology and Medical Embryology, Sapienza University of Rome, 00161 Rome, Italy.

Department of Anatomy, Histology, Forensic Medicine and Orthopaedics, Unit of Human Anatomy, Sapienza University of Rome, 00161 Rome, Italy.

出版信息

Biomolecules. 2020 Sep 30;10(10):1398. doi: 10.3390/biom10101398.

DOI:10.3390/biom10101398
PMID:33008140
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7601508/
Abstract

Autophagy is an evolutionary conserved and highly regulated recycling process of cellular wastes. Having a housekeeping role, autophagy through the digestion of domestic cytosolic organelles, proteins, macromolecules, and pathogens, eliminates unnecessary materials and provides nutrients and energy for cell survival and maintenance. The critical role of autophagy and autophagy-related proteins in osteoclast differentiation, bone resorption, and maintenance of bone homeostasis has previously been reported. Increasing evidence reveals that autophagy dysregulation leads to alteration of osteoclast function and enhanced bone loss, which is associated with the onset and progression of osteoporosis. In this review, we briefly consolidate the current state-of-the-art technology regarding the role of autophagy in osteoclast function in both physiologic and pathologic conditions to have a more general view on this issue.

摘要

自噬是一种进化上保守且高度调控的细胞废物回收过程。自噬作为一种管家功能,通过消化细胞内的细胞质细胞器、蛋白质、大分子和病原体,消除不必要的物质,并为细胞的生存和维持提供营养和能量。自噬和自噬相关蛋白在破骨细胞分化、骨吸收和维持骨稳态中的关键作用以前已有报道。越来越多的证据表明,自噬失调导致破骨细胞功能改变和骨丢失增强,这与骨质疏松症的发生和进展有关。在这篇综述中,我们简要总结了自噬在生理和病理条件下对破骨细胞功能的作用的最新技术现状,以便更全面地了解这个问题。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3599/7601508/15d24658c2f5/biomolecules-10-01398-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3599/7601508/7033e1216389/biomolecules-10-01398-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3599/7601508/15d24658c2f5/biomolecules-10-01398-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3599/7601508/7033e1216389/biomolecules-10-01398-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3599/7601508/15d24658c2f5/biomolecules-10-01398-g002.jpg

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Deletion of p16 prevents estrogen deficiency-induced osteoporosis by inhibiting oxidative stress and osteocyte senescence.p16基因的缺失通过抑制氧化应激和骨细胞衰老来预防雌激素缺乏诱导的骨质疏松症。
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Autophagy promotes osteoclast podosome disassembly and cell motility athrough the interaction of kindlin3 with LC3.
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