Department of Rehabilitation Medicine, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, People's Republic of China.
Key Laboratory of Rehabilitation Medicine, West China Hospital, Sichuan University, Chengdu, People's Republic of China.
Apoptosis. 2020 Apr;25(3-4):157-168. doi: 10.1007/s10495-020-01599-0.
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.
糖皮质激素被广泛用于治疗各种过敏性和自身免疫性疾病；然而，长期使用会导致糖皮质激素诱导的骨质疏松症，其特征是骨重建持续变化，骨形成减少，骨吸收增加。不仅骨量减少，而且骨质量下降，导致骨折发生率增加。自噬的主要作用是清除如长寿蛋白和细胞器等受损的细胞成分，从而参与不同细胞的保护。细胞凋亡是细胞的生理性死亡，在组织内环境的稳定性中起着关键作用。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。在这篇综述中，我们总结了与糖皮质激素相关的细胞凋亡、自噬与骨代谢之间的关系，为治疗靶点提供了理论依据，以挽救糖皮质激素诱导的骨质疏松症中的骨量和骨质量。
