Purpose Androgenetic alopecia, commonly known as male pattern baldness, is the most common type of progressive hair loss disorder in men. The aim of this paper is to review recent advances in understanding the pathophysiology and molecular mechanism of androgenetic alopecia. Methods Using the PubMed database, we conducted a systematic review of the literature, selecting studies pub- lished from 1916 to 2016. Results The occurrence and development of androgenetic alopecia depends on the interaction of endocrine factors and genetic predisposition. Androgenetic alopecia is character- ized by progressive hair follicular miniaturization, caused by the actions of androgens on the epithelial cells of genetically susceptible hair follicles in androgen-dependent areas. Although the exact pathogenesis of androgenetic alopecia remains to be clari fi ed, research has shown that it is a polygenetic condition. Numerous studies have unequi- vocally identi fi ed two major genetic risk loci for androge- netic alopecia, on the X-chromosome AR ⁄ EDA2R locus and the chromosome 20p11 locus. Conclusions Candidate gene and genome-wide association studies have reported that single-nucleotide polymorphisms at different genomic loci are associated with androgenetic alopecia development. A number of genes determine the predisposition for androgenetic alopecia in a polygenic fashion. However, further studies are needed before the specific genetic factors of this polygenic condition can be fully explained

Androgenetic alopecia: a review / Lolli, Francesca; Pallotti, Francesco; Rossi, Alfredo; Fortuna, MARIA CATERINA; Caro, Gemma; Lenzi, Andrea; Sansone, Andrea; Lombardo, Francesco. - In: ENDOCRINE. - ISSN 1355-008X. - ELETTRONICO. - 57:1(2017), pp. 9-17. [10.1007/s12020-017-1280-y]

Androgenetic alopecia: a review

LOLLI, FRANCESCA
Primo
;
PALLOTTI, FRANCESCO
Secondo
;
ROSSI, Alfredo;FORTUNA, MARIA CATERINA;CARO, GEMMA;LENZI, Andrea;LOMBARDO, Francesco
Ultimo
2017

Abstract

Purpose Androgenetic alopecia, commonly known as male pattern baldness, is the most common type of progressive hair loss disorder in men. The aim of this paper is to review recent advances in understanding the pathophysiology and molecular mechanism of androgenetic alopecia. Methods Using the PubMed database, we conducted a systematic review of the literature, selecting studies pub- lished from 1916 to 2016. Results The occurrence and development of androgenetic alopecia depends on the interaction of endocrine factors and genetic predisposition. Androgenetic alopecia is character- ized by progressive hair follicular miniaturization, caused by the actions of androgens on the epithelial cells of genetically susceptible hair follicles in androgen-dependent areas. Although the exact pathogenesis of androgenetic alopecia remains to be clari fi ed, research has shown that it is a polygenetic condition. Numerous studies have unequi- vocally identi fi ed two major genetic risk loci for androge- netic alopecia, on the X-chromosome AR ⁄ EDA2R locus and the chromosome 20p11 locus. Conclusions Candidate gene and genome-wide association studies have reported that single-nucleotide polymorphisms at different genomic loci are associated with androgenetic alopecia development. A number of genes determine the predisposition for androgenetic alopecia in a polygenic fashion. However, further studies are needed before the specific genetic factors of this polygenic condition can be fully explained
2017
AGA; AGA genetics; androgen metabolism; androgen receptor; finasteride; male pattern baldness; endocrinology, diabetes and metabolism; endocrinology
01 Pubblicazione su rivista::01g Articolo di rassegna (Review)
Androgenetic alopecia: a review / Lolli, Francesca; Pallotti, Francesco; Rossi, Alfredo; Fortuna, MARIA CATERINA; Caro, Gemma; Lenzi, Andrea; Sansone, Andrea; Lombardo, Francesco. - In: ENDOCRINE. - ISSN 1355-008X. - ELETTRONICO. - 57:1(2017), pp. 9-17. [10.1007/s12020-017-1280-y]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/951564
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