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Glucocorticoid-induced autophagy and apoptosis in bone.
Apoptosis ( IF 7.2 ) Pub Date : 2020-04-01 , DOI: 10.1007/s10495-020-01599-0
Tiantian Wang 1, 2 , Xiaonan Liu 3 , Chengqi He 1, 2
Affiliation  

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.

中文翻译:

糖皮质激素诱导的骨骼肌自噬和细胞凋亡。

糖皮质激素被广泛处方用于治疗各种变应性和自身免疫性疾病。然而,长期使用会导致糖皮质激素诱发的骨质疏松症,其特征是骨骼重塑的持续变化与减少的骨形成以及增加的骨吸收有关。不仅骨头质量下降,而且骨头质量下降,导致骨折的发生率增加。自噬的主要作用是清除受损的细胞成分,例如长寿的蛋白质和细胞器,从而参与保存不同的细胞。凋亡是细胞的生理死亡,并且在组织内部环境的稳定性中起关键作用。现有的基础和临床研究表明,糖皮质激素诱导的自噬和细胞凋亡可以通过复杂的机制调节骨代谢。在这篇评论中
更新日期:2020-04-20
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