Abstract
Androgenetic alopecia (AGA) is mainly characterized by androgen-dependent follicular miniaturization. However, increasing evidence suggests that inflammation, fibrosis and vascular changes may also affect the follicular microenvironment. This review summarizes the normal vascular and cellular regulation of the hair follicle and discusses how these processes may be altered in AGA. Human studies have identified perifollicular inflammation, reduced perfusion and changes in angiogenesis-related genes, but their causal roles remain unclear. Experimental studies further show close communication among dermal papilla cells, endothelial cells, immune cells and hair follicle stem cells. Current treatments mainly reduce androgen signaling or stimulate hair growth and may not fully address these microenvironmental changes. Emerging approaches, including anti-inflammatory treatments, nitric oxide and VEGF-based systems, microneedles, hydrogels and nano-enabled delivery, may regulate several pathways at the same time. However, most of these strategies remain preclinical. Future studies should clarify whether inflammation and vascular dysfunction are causes or consequences of follicular miniaturization and determine whether targeting these pathways can improve clinical outcomes in AGA.