Summary
Several journal reports, reviews, and commentaries over the last 20‐25 years have pointed out the controversy attached to 17β‐estradiol's inhibitory or stimulatory influence on hair follicle growth/cycling citing rodent (murine) and human results. While 17β‐estradiol is the most potent sex steroid hormone in the body and has almost equal affinity for estrogen receptor (ER) alpha (α) and beta (β), there appears to be specific ER‐mediated effects on scalp hair follicles/growth, etc. Additionally, the newly discovered G protein‐coupled estrogen receptor (GPR30 or GPER) and the orphan receptor, estrogen‐related receptor (ERR) gamma (γ), in skin and other tissue sites have potential impacts of how estrogens via these receptors may alter scalp hair characteristics, but this remains to be elucidated. Conversely, the negative impact of the 5α‐reductase enzyme and its steroid product, 5α‐dihydrotestosterone, on scalp hair growth is clear. Less clear is how 17β‐estradiol is stimulatory in some scalp hair studies, but inhibitory in others. This brief summary examines the potential influences of steroidogenesis via aromatase (estrogen biosynthesis) and 5α‐reductase expression, their enzyme activities, and steroid products along with the concepts of how steroid acute regulatory protein (StAR) and estrone sulfate may be involved in the complex hormonal, cellular/molecular signaling cascade of the hair follicle in growth and cycling.
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