The Critical Role of Autophagy in the Pathogenesis of Diabetic Osteoporosis: Mechanisms and Therapeutic Measures.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

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 therapeu

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.