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已发表论文
自噬在糖尿病性骨质疏松症发病机制中的关键作用：机制与治疗措施
Authors Hou K , Shi W, Xu K, Wang T, Zhang Y
Received 17 July 2025
Accepted for publication 27 October 2025
Published 6 November 2025 Volume 2025:19 Pages 9913—9942
DOI https://doi.org/10.2147/DDDT.S554555
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Tuo Deng
Kehao Hou,* Weipeng Shi,* Kuishuai Xu, Tianrui Wang, Yingze Zhang
Knee Preservation Center, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Tianrui Wang, Knee preservation center, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, 266000, People’s Republic of China, Tel +8613589299775; +8618533212888, Email wtrabc123@126.com Yingze Zhang, Knee preservation center, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, 266000, People’s Republic of China, Tel +8613589299775; +8618533212888, Email acadyzzhang@126.com
Abstract: Diabetic osteoporosis (DOP) represents a significant skeletal complication of diabetes mellitus characterized by compromised bone quality and increased fracture risk. Autophagy, a conserved cellular homeostatic mechanism, serves as a key regulator of bone formation and resorption balance. This review comprehensively examines the pivotal role of autophagy in DOP pathogenesis and explores emerging therapeutic strategies targeting autophagic regulation. Under hyperglycemic conditions, dysregulated autophagy occurs through multiple signaling pathways, including ROS-mTOR, PINK1/Parkin-mediated mitophagy, FoxO transcription factors, AGEs-RAGE and TLR4/NF-κB cascades etc. These disturbances manifest distinctly in various cell types: impaired mineralization of osteoblasts, altered bone resorption of osteoclasts, compromised insulin secretion of pancreatic β-cells, diminished osteogenic differentiation of bone marrow mesenchymal stem cells and adipose-derived stem cells. Current therapeutic approaches targeting autophagy dysregulation include pharmacological interventions such as metformin, rapamycin and vitamin D analogs, autophagy enhancers such as resveratrol and AMPK activators, specific inhibitors regulating excessive autophagic activity, Chinese medicinal compounds and exercise regimens. Emerging strategies also include gene therapy, stem cell transplantation and combined therapeutic approaches that precisely modulate the dynamic balance of autophagic flux. Moreover, we underscore the critical importance of maintaining optimal autophagic activity—neither excessive nor insufficient—in bone cells to preserve metabolic homeostasis and prevent osteoporotic progression in DOP patients. Future research directions should focus on elucidating specific mechanisms of action, identifying optimal intervention timing and exploring synergistic therapeutic combinations to effectively manage this challenging metabolic bone disorder.
Keywords: diabetes, osteoporosis, autophagy, mechanism, therapeutic strategies
Knee Preservation Center, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Tianrui Wang, Knee preservation center, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, 266000, People’s Republic of China, Tel +8613589299775; +8618533212888, Email wtrabc123@126.com Yingze Zhang, Knee preservation center, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, 266000, People’s Republic of China, Tel +8613589299775; +8618533212888, Email acadyzzhang@126.com
Abstract: Diabetic osteoporosis (DOP) represents a significant skeletal complication of diabetes mellitus characterized by compromised bone quality and increased fracture risk. Autophagy, a conserved cellular homeostatic mechanism, serves as a key regulator of bone formation and resorption balance. This review comprehensively examines the pivotal role of autophagy in DOP pathogenesis and explores emerging therapeutic strategies targeting autophagic regulation. Under hyperglycemic conditions, dysregulated autophagy occurs through multiple signaling pathways, including ROS-mTOR, PINK1/Parkin-mediated mitophagy, FoxO transcription factors, AGEs-RAGE and TLR4/NF-κB cascades etc. These disturbances manifest distinctly in various cell types: impaired mineralization of osteoblasts, altered bone resorption of osteoclasts, compromised insulin secretion of pancreatic β-cells, diminished osteogenic differentiation of bone marrow mesenchymal stem cells and adipose-derived stem cells. Current therapeutic approaches targeting autophagy dysregulation include pharmacological interventions such as metformin, rapamycin and vitamin D analogs, autophagy enhancers such as resveratrol and AMPK activators, specific inhibitors regulating excessive autophagic activity, Chinese medicinal compounds and exercise regimens. Emerging strategies also include gene therapy, stem cell transplantation and combined therapeutic approaches that precisely modulate the dynamic balance of autophagic flux. Moreover, we underscore the critical importance of maintaining optimal autophagic activity—neither excessive nor insufficient—in bone cells to preserve metabolic homeostasis and prevent osteoporotic progression in DOP patients. Future research directions should focus on elucidating specific mechanisms of action, identifying optimal intervention timing and exploring synergistic therapeutic combinations to effectively manage this challenging metabolic bone disorder.
Keywords: diabetes, osteoporosis, autophagy, mechanism, therapeutic strategies