4.4 Article

Evaluation of serum G protein-coupled estrogen receptor 1 (GPER-1) levels in patients with androgenetic alopecia

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ARCHIVES OF DERMATOLOGICAL RESEARCH
卷 314, 期 7, 页码 681-685

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SPRINGER
DOI: 10.1007/s00403-021-02269-0

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Androgenetic alopecia; Inflammation; Estrogen receptor; GPER-1

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This study found significantly increased serum GPER-1 levels in AGA patients, suggesting that GPER-1 may play a role in AGA pathogenesis independent from gender.
The effect of oestrogens in androgenetic alopecia (AGA) pathophysiology has not been clearly understood. However, they are considered to have a place in the AGA pathogenesis as the androgens do. The effects of estrogen occur via the estrogen receptors alpha and beta, and the recently discovered G protein-coupled estrogen receptor 1 (GPER-1). Aim of this study is to examine serum GPER-1 levels of AGA patients and to evaluate the place of them in AGA pathogenesis for the first time through the literature. 40 AGA patients with clinical AGA stage 2-3-4 diagnoses according to the Hamilton-Norwood classification for males, and AGA stage 2 according to Ludwig system for females and with normal serum dihydroepiandrosterone sulfate, estradiol, total testosterone, progesterone, follicle stimulating hormone and luteinizing hormone were included in the study in addition to 40 healthy controls with similar characteristics by means of age and gender. We received the medical history and performed the physical examinations. We measured serum GPER-1 levels. Serum GPER-1 levels of AGA patients and the control group were 30.43 +/- 3.83 ng/mL and 14.18 +/- 3.61 ng/mL (mean +/- SD), respectively. The levels were detected as significantly increased in AGA group compared with the control group (p=0.007). No serum GPER-1 level differences were found among female and male patients (p=0.101). Significantly high levels of serum GPER-1 levels in AGA patients without any relationship between gender and GPER-1 Levels compared with healthy controls reminded us that GPER-1 might have a role in AGA pathogenesis independent from the gender.

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