Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2021 May 12;12:675385. doi: 10.3389/fendo.2021.675385

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2021 Da, Tao and Zhu

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Hypothesis of the compensatory recovery mechanism of osteoclasts. (A) Based on proapoptotic BIM and anti-apoptotic BCL-xL, an imbalance between osteoclast survival and bone resorptive capacity occurs in OP. (B) The disruption of homeostasis between the enhancement of bone resorption activity mediated by hypoxia and the inhibition of ROS on the survival of osteoclasts promotes the occurrence of osteoporosis. (C) RANKL-mediated oxidative stress results in an imbalance between osteoclast survival and bone resorption capacity. ATP, adenosine triphosphate; BCL-xL, B-cell lymphoma-extra large; BIM, BCL-2-like protein 11; HIF-1, hypoxia-induced factor-1; OP, osteoporosis; ROS, reactive oxygen species; RANKL, receptor activator of nuclear factor kappa-B ligand; SOD2, superoxide dismutase 2.