Mechanism of Methylglyoxal-Induced Oxidative Stress Injury in Diabetic Osteoporosis

Résumé fourni par la source

Diabetic osteoporosis (DOP) is a severe chronic complication of diabetes affecting the skeletal system. Its incidence has been increasing year by year with the rising global prevalence of diabetes, making it a significant public health issue that threatens the quality of life of diabetic patients. Methylglyoxal (MG), a highly reactive carbonyl compound, accumulates abnormally under the hyperglycemic microenvironment in diabetes and serves as a key mediator linking glucose metabolism disorder with bone metabolic imbalance. Numerous basic and clinical studies have confirmed that MG-induced oxidative stress injury in bone cells is a core pathological link in the development and progression of DOP. Osteoblasts and osteoclasts serve as the two key effector cells that regulate bone homeostasis. However, these two cell types exhibit distinct cell-specific responses to MG and oxidative stress, and the underlying molecular regulatory networks remain largely unclear. This review systematically summarizes the pathophysiological role of MG in DOP. It focuses on the regulatory mechanisms by which MG accumulation induces both oxidative stress and mitochondrial dysfunction, two processes that mutually reinforce each other, ultimately leading to aberrant function of osteoblasts and osteoclasts. In-depth elucidation of the molecular mechanisms underlying MG-induced oxidative stress injury in bone cells will provide new theoretical support and potential intervention targets for the prevention and treatment of DOP, with significant value for basic research and clinical translation.

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