Abstract:

Clarifying the sources and elimination pathways of advanced glycation end products （AGEs） is of great necessity for the development of anti-glycation cosmetics. This paper summarizes findings from studies on influencing factors of AGE formation, AGE synthesis, cellular responses, and degradation. It reveals that both endogenous and exogenous factors affect AGE synthesis by modulating blood glucose levels, AGE degradation efficiency, and inflammatory responses. The synthetic pathways involve traditional routes such as the polyol and glycolytic pathways, as well as non-traditional mechanisms including the Maillard reaction, acetol pathway, and glucose autoxidation. AGEs induce mechanical alterations in collagen fibers or stimulate cellular responses through interactions with receptors like RAGE, members of the AGE-R family, and the NF-κB signaling pathway. AGE degradation occurs via recognition by AGE-R or endocytosis, followed by breakdown mediated by cellular metabolic enzyme systems, with subsequent elimination through blood circulation or urinary excretion. Consequently, strategies aimed at suppressing AGE accumulation in the skin provide a theoretical foundation for the targeted development of anti-glycation cosmetics.

Key words: non-enzymatic glycation, influencing factors, synthesis, cellular response, degradation