Journal
JOURNAL OF CELLULAR PHYSIOLOGY
Volume 236, Issue 9, Pages 6691-6705Publisher
WILEY
DOI: 10.1002/jcp.30331
Keywords
dexamethasone; EC‐ Exos; ferroptosis; osteoporosis
Categories
Funding
- National Natural Science Foundation of China [81672206]
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High dose and long-term steroid treatment can lead to osteoporosis and osteonecrosis by altering antioxidative ability and inducing excessive lipid peroxidation through pathways like ferroptosis. Endothelial cell-secreted exosomes play a protective role in glucocorticoid-induced osteoporosis by inhibiting ferroptosis-dependent osteogenic inhibition of osteoblasts.
High dose and long-term steroid treatment can alter antioxidative ability and decrease the viability and function of osteoblasts, leading to osteoporosis and osteonecrosis. Ferroptosis, a new type of cell death characterized by excessive lipid peroxidation due to the downregulation of GPX4 and system Xc-, is involved in glucocorticoid-induced osteoporosis. Endothelial cell-secreted exosomes (EC-Exos) are important mediators of cell-to-cell communication and are involved in many physiological and pathological processes. However, the effect of EC-Exos on osteoblasts exposed to glucocorticoids has not been reported. Here, we explored the role of EC-Exos in glucocorticoid-induced osteoporosis. In vivo and in vitro experiments indicated that EC-Exos reversed the glucocorticoid-induced osteogenic inhibition of osteoblasts by inhibiting ferritinophagy-dependent ferroptosis.
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