Advanced glycation end products (AGEs) are stable glycosylation products formed after oxidation, dehydration, condensation, isomerization and cyclization between lipids, proteins, nucleic acids and free groups of reduced sugars, which can participate in the regulation of many metabolic diseases in the elderly. In recent years, with the deepening of the research and exploration of high glucose-induced AGEs, it is found that it is closely related to the maintenance of "muscle bone homeostasis" and participates in the formation and development of myosseous attenuation diseases. Sarcopenia-osteoporosis (osteosarcopenia,OS) is a senile metabolic disease characterized by bone density, pathological loss of muscle mass and function, which seriously threatens the physical and mental health of the elderly; which is prone to fragility fracture, disability and even death. Therefore, this paper discusses the effects of AGEs on sarcopenia-osteoporosis through N6-methyadenosine, DNA methylation, autophagy, iron death, RANKL/RANK pathway, space microgravity pathway, RAGE /AGEs pathway, glycan crosslinking, aiming to explore the mechanism of high glucose-induced AGEs in intervening sarcopenia-osteoporosis, in order to provide new ideas for regulating "muscle bone homeostasis". |