94 citations
,
August 2002 in “Experimental Dermatology” This study found that 17α‐estradiol increases aromatase activity in female hair follicles, which may explain its beneficial effects in treating androgenetic alopecia.
12 citations
,
August 2002 in “Archives of Dermatology”
19 citations
,
June 2002 in “American Journal of Dermatopathology” This study found significant differences in bcl-2 expression between areas of the scalp affected and unaffected by androgenetic alopecia, suggesting a uniform follicle population or synchronized follicular cycling in affected areas.
61 citations
,
December 2001 in “Journal of Investigative Dermatology” This study found that steroid sulfatase in the dermal papilla of hair follicles metabolizes dehydroepiandrosterone sulfate to support the development of androgenetic alopecia, suggesting potential for steroid sulfatase inhibitors as treatments.
116 citations
,
September 2001 in “Journal of The American Academy of Dermatology” This study suggests that miniaturization in pattern hair loss may occur abruptly and can be reversed with treatment, as supported by histologic evidence in finasteride-responsive patients.
23 citations
,
August 2001 in “PubMed” In this study, finasteride treatment in men with androgenetic alopecia reduced the expression of caspases in hair follicles to levels similar to those in men with normal scalps.
28 citations
,
February 1999 in “Archives of Dermatological Research” Finasteride potentially treats hair loss by reducing DHT production.
51 citations
,
November 1998 in “The journal of investigative dermatology/Journal of investigative dermatology” In this study, researchers found that while both beard and scalp dermal papilla cells release similar autocrine growth factors, only beard cells increased production and response with testosterone, suggesting these factors enhance androgen-induced hair growth.
March 1998 in “Journal of dermatological science” Protease Nexin-1 is found in human hair growth cells and is affected by male hormones.
416 citations
,
September 1997 in “Journal of Investigative Dermatology” People with hair loss have more androgen receptors and enzymes in certain follicles, with men and women showing different patterns.
33 citations
,
January 1997 in “Endocrinology” Testosterone was found to inhibit hair follicle epithelial cell proliferation in adult stumptailed macaques only when dermal papilla cells from bald scalps were present, and this effect was reversed by the antiandrogen RU 58841.
37 citations
,
December 1995 in “Journal of Cell Science” This study found that nexin 1 mRNA, a potent protease inhibitor, is prevalent in rat follicular papilla cells and may play a role in regulating hair follicular growth.
25 citations
,
July 1994 in “Journal of dermatological science” This study observed that testosterone metabolism and androgen receptor localization differ significantly across body sites, with beard hair follicles showing distinct characteristics compared to occipital scalp hair follicles.
34 citations
,
December 1991 in “Annals of the New York Academy of Sciences” This study found that while the steroid mechanisms influencing androgenetic alopecia may be similar for men and women, differences in enzyme activity and receptor content could explain their varied clinical presentations.
22 citations
,
July 1990 in “Acta Dermato Venereologica” In this study, high concentrations of dihydrotestosterone and testosterone reduced the growth of human hair follicle cells in vitro, while high estradiol levels increased their growth.
8 citations
,
September 1987 in “Acta Dermato Venereologica” In this study, the researchers used structural studies and molecular calculations to suggest that the enzyme in RXLI patient hair follicles is less efficient, rather than completely inactive.
52 citations
,
March 1987 in “Journal of the American Academy of Dermatology” This study found that men with rapidly progressive male pattern baldness had elevated serum dehydroepiandrosterone sulfate levels, suggesting that adrenal hyperactivity may contribute to alopecia in genetically susceptible young men.