The role of wnt signaling in diabetes-induced osteoporosis

Osteoporosis, a chronic complication of diabetes mellitus, is characterized by a reduction in bone mass, destruction of bone microarchitecture, decreased bone strength, and increased bone fragility. Because of its insidious onset, osteoporosis renders patients highly susceptible to pathological fractures, leading to increased disability and mortality rates. However, the specific pathogenesis of osteoporosis induced by chronic hyperglycemia has not yet been fully elucidated. But it is currently known that the disruption of Wnt signaling triggered by chronic hyperglycemia is involved in the pathogenesis of diabetic osteoporosis. There are two main types of Wnt signaling pathways, the canonical Wnt signaling pathway (beta-catenin-dependent) and the non-canonical Wnt signaling pathway (non-beta-catenin-dependent), both of which play an important role in regulating the balance between bone formation and bone resorption. Therefore, this review systematically describes the effects of abnormal Wnt pathway signaling on bone homeostasis under hyperglycemia, hoping to reveal the relationship between Wnt signaling and diabetic osteoporosis to further improve understanding of this disease.

Automated summary

Osteoporosis, a chronic complication of diabetes mellitus, is caused by chronic hyperglycemia-induced disruption of Wnt signaling pathways. The canonical and non-canonical Wnt signaling pathways play a crucial role in regulating bone homeostasis. This review aims to provide a comprehensive understanding of the effects of abnormal Wnt pathway signaling on bone under hyperglycemia, shedding light on the pathogenesis of diabetic osteoporosis.