Spontaneous Coronary Artery Dissection and Takotsubo Syndrome: Converging Mechanisms, Diagnostic Pitfalls, and a Unified Clinical Algorithm.

Androgenetic alopecia (AGA), as the leading cause of non‐cicatricial alopecia, has contributed to an increasing disease burden worldwide in recent years []. The global prevalence among men is approximately 20%–50%, affecting up to half of Caucasian men over the age of 50 []. It is typically characterized by a receding hairline that begins in the frontal and temporal scalp and may progress to the vertex []. Beyond its physical manifestations, AGA can significantly impact psychological well‐being, leading to reduced self‐esteem, anxiety, depression, and other emotional concerns []. However, the current management of AGA continues to face multiple challenges []. Although commonly used pharmacological treatments such as finasteride and minoxidil demonstrate certain efficacy, their effectiveness remains suboptimal and is associated with notable limitations [, ]. In particular, anti‐androgen therapies represented by finasteride exhibit considerable heterogeneity in treatment response among patients, suggesting that mechanisms beyond androgen signaling may play significant roles in the pathogenesis of AGA []. Despite diverse basic research on hair follicle development and cycling, the precise etiology underlying this common condition remains incompletely elucidated [, , ]. Moreover, the cellular heterogeneity within hair follicles and the cell type‐specific molecular alterations in hair follicle stem cells (HFSCs) during AGA remain poorly understood. Consequently, further investigation into the underlying pathogenic mechanisms of AGA and the identification of potential therapeutic targets are of critical importance. As the primary structure involved in hair loss, the hair follicle (HF) possesses a highly complex architecture and microenvironment []. The HF cycle progresses through phases of anagen, catagen, and telogen []. Mice exhibiting synchronized hair growth waves serve as valuable models for HF research, and studies in mice have elucidated hair lineage dynamics originating from adult stem cells residing in the HF bulge (BG) and hair germ (HG) [, ]. To date, much of our understanding of AGA mechanisms derives from mechanistic studies in murine models []. However, a detailed molecular atlas of the human hair follicle remains unelucidated, and no study has yet comprehensively explored the specific molecular alterations across distinct cell populations within balding HFs of AGA patients. Identifying key molecular changes in HFs from affected areas is essential for clarifying the underlying pathogenic mechanisms of AGA.