Advanced Glycation End-Products Inhibit Mesenchymal-Epidermal Interaction by Up-Regulating Proinflammatory Cytokines in Hair Follicles

The document detailed a study on the impact of advanced glycation end-products (AGEs) on hair follicle function and their potential connection to alopecia. AGEs accumulate with age and are known to damage cellular functions, contributing to aging-related diseases. The study found that AGEs in the dermal papilla of mouse skin suppressed the proliferation of human primary keratinocytes through conditioned media from dermal papilla cells (DPCs). This suppression was not due to a direct effect on keratinocytes and DPCs, but rather through the up-regulation of pro-inflammatory cytokines (IL-1α, IL-1ß, IL-6, IL-8, and TNF-α) in DPCs, mediated by the ROS-mediated NF-kB pathway. The results suggest that AGEs may promote androgenetic alopecia and trigger hair follicle senescence, leading to age-related hair loss. The study proposes that targeting hair follicular AGEs could be a strategy to prevent age-related hair issues. The document did not disclose the number of participants or samples, financial support, or conflicts of interest.