Mechanisms of AGEs induced ovarian cellular senescence.Firstly, AGEs, upon binding to its receptors (RAGE), triggers inflammatory signaling pathways, leading to the upregulation of ROS and SASPs. This cascade results in inflammation, oxidative stress and DNA damage, ultimately leading to cellular senescence. Additionally, ROS can enhance AGEs formation, and the interaction of AGEs with RAGE can further upregulate RAGE expression, perpetuating a vicious cycle. Secondly, another AGE receptor sRAGE, prevents excess ligand from binding to RAGE, thereby protecting cells from damage caused by the AGEs-induced inflammatory cascade. Thirdly, AGEs promote cellular senescence by upregulating abnormal collagen cross-linking and ECM formation in the ovaries. The SASPs produced by senescent cells also promotes ECM accumulation, thereby exacerbating cellular senescence.