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. 2021 Jul 14;12:722175. doi: 10.3389/fphar.2021.722175

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Copyright © 2021 Lai, Mo, Wang, Zhong, Lu, Wang, Cui, Liu and Yang.

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.

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Model of the pathogenesis of GC-induced microcirculation dysfunction and impaired osteogenesis by TXNIP and its intervention of tanshinol: Long-term high-dose glucocorticoid can activate expression of TXNIP proteins. TXNIP down-regulates both VEGF and Wnt signaling pathways in vascular endothelial cells and osteoblasts respectively, contributing to inhibition of angiogenesis, followed by dysfunction of microcirculation in bone vessels, which causes blood stasis and decreased bone formation and eventually induced osteoporosis. However, tanshinol protects rats from GIO involving in the regulation of TXNIP/Wnt/VEGF cascade pathway.