Glucocorticoid-induced autophagy and apoptosis in bone

Apoptosis : an International Journal on Programmed Cell Death
Tiantian WangChengqi He

Abstract

Glucocorticoids are widely prescribed to treat various allergic and autoimmune diseases; however, long-term use results in glucocorticoid-induced osteoporosis, characterized by consistent changes in bone remodeling with decreased bone formation as well as increased bone resorption. Not only bone mass but also bone quality decrease, resulting in an increased incidence of fractures. The primary role of autophagy is to clear up damaged cellular components such as long-lived proteins and organelles, thus participating in the conservation of different cells. Apoptosis is the physiological death of cells, and plays a crucial role in the stability of the environment inside a tissue. Available basic and clinical studies indicate that autophagy and apoptosis induced by glucocorticoids can regulate bone metabolism through complex mechanisms. In this review, we summarize the relationship between apoptosis, autophagy and bone metabolism related to glucocorticoids, providing a theoretical basis for therapeutic targets to rescue bone mass and bone quality in glucocorticoid-induced osteoporosis.

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Citations

Apr 23, 2020·International Journal of Molecular Sciences·Viviana di GiacomoSilvia Sancilio

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Methods Mentioned

BETA
gene array

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