The regulatory mechanisms of mitophagy and oxidative stress in androgenetic alopecia.

Androgenetic alopecia (AGA), the most common type of non-scarring hair loss in dermatology, result from a multifaceted interplay of genetic susceptibility, abnormal androgen metabolism, and dysregulation within the follicular microenvironment. Recent studies have highlighted the crucial roles of mitophagy and oxidative stress in the pathogenesis and progression of AGA. Mitophagy, a selective process by which damaged mitochondria are eliminated, is essential for maintaining cellular energy metabolism homeostasis and redox balance. In contrast, oxidative stress results from excessive accumulation of reactive oxygen species (ROS), which induces cellular damage and accelerates disease progression. The disruption of the dynamic balance between mitophagy and oxidative stress is increasingly recognized as a key factor in the development and exacerbation of AGA. Despite initial studies elucidating the interaction between these two processes, the precise molecular mechanisms and regulatory networks governing AGA remain insufficiently understood. This review aims to systematically synthesize the latest findings concerning the interplay between mitophagy and oxidative stress in AGA. By examining their roles in the disease's onset and progression, we identify potential therapeutic targets for intervention. Additionally, we discuss relevant signaling pathways and cellular mechanisms, evaluating the therapeutic potential of targeting mitophagy and oxidative stress for the treatment of AGA.