Glucocorticoid-induced autophagy and apoptosis in bone
Tiantian Wang1,2, Xiaonan Liu3, Chengqi He4,5
1Department of Rehabilitation Medicine, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, People's Republic of China.
Summary
Glucocorticoids cause osteoporosis by disrupting bone remodeling. This review explores how apoptosis and autophagy influence bone metabolism, offering insights for treating glucocorticoid-induced osteoporosis.
Area of Science:
- Biomedical Science
- Cell Biology
- Bone Metabolism
Background:
- Glucocorticoids are commonly prescribed for allergic and autoimmune diseases.
- Long-term use leads to glucocorticoid-induced osteoporosis, marked by reduced bone formation and increased resorption.
- This results in decreased bone mass, impaired bone quality, and elevated fracture risk.
Purpose of the Study:
- To review the complex mechanisms linking glucocorticoid-induced apoptosis and autophagy to bone metabolism.
- To provide a theoretical foundation for developing therapeutic strategies against glucocorticoid-induced osteoporosis.
Main Methods:
- Literature review of basic and clinical studies.
- Analysis of the roles of apoptosis and autophagy in glucocorticoid action on bone.
Main Results:
- Glucocorticoids induce both apoptosis and autophagy, significantly impacting bone remodeling.
- These cellular processes are key regulators of bone metabolism under glucocorticoid influence.
- Understanding these pathways is crucial for addressing bone loss.
Conclusions:
- Apoptosis and autophagy are central to glucocorticoid-induced osteoporosis.
- Targeting these pathways may offer novel therapeutic approaches to restore bone mass and quality.
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