Background: Both men and women can experience androgenetic alopecia (AGA), a common type of hair loss. The miniaturization of hair follicles results from a complex interplay involving inflammatory agents, hormones, and genetic predisposition. Advanced Glycation End Products (AGEs) and their receptors (RAGE) have emerged as potential contributors to the pathophysiology of AGA, linking inflammation and oxidative stress to hair follicle changes.
Objective: This review aims to explore the relationship between AGA pathogenesis, RAGE production, and serum AGE levels. It investigates the potential utility of AGEs and RAGE as either diagnostic markers or therapeutic targets, elucidating the molecular pathways through which they impact follicular miniaturization and subsequent hair loss.
Conclusions: The investigation reveals AGEs and their receptors as pivotal in AGA's development, exacerbating hair follicle miniaturization via oxidative stress and inflammation. AGE-induced RAGE activation triggers cascading inflammatory responses, disrupting the follicular environment. Understanding these molecular interactions opens avenues for novel diagnostics and targeted treatments to mitigate hair loss in affected individuals.