AI Article Synopsis

  • Androgenetic alopecia (AGA) is a prevalent form of hair loss affecting around 50% of men, prompting research into its underlying mechanisms.
  • The study measured various serum biomarkers in 58 AGA patients and 30 healthy controls, finding significantly elevated levels of inflammation and oxidative stress markers in AGA patients compared to controls.
  • Results suggest that androgens may contribute to hair loss in AGA by inducing oxidative stress and inflammation, highlighting the need for new treatment strategies targeting these factors.

Article Abstract

Background: Androgenetic alopecia (AGA) is the most common type of hair loss and affects approximately 50% of the male population.

Aims: In the present study, to investigate microinflammation, perifollicular fibrosis, and oxidative stress in AGA cases, some serum biomarker levels were measured and evaluated.

Patients/methods: Serum samples were drawn from patients (n = 58) and control (n = 30) groups referring to Atatürk Training and Investigation Hospital Dermatology Outpatient clinic. In serum samples, NF-κB, TNF-α, TGF-β1, thioredoxin, nitric oxide, TOS, TAS, and thiol disulfide homeostasis (native thiol, total thiol, disulfide) were measured and evaluated.

Results: In patients with AGA, NF-κB (P = .005), TNF-α (P = .008), TGF-β1 (P = .028), thioredoxin (P = .004), nitric oxide (P < .001), and TOS (P < .001) serum levels were found to be significantly higher than those in control group, while TAS (P = .003), native thiol (P < .001), total thiol (P < .001), and disulfide (P < .001) serum levels were found to be significantly lower.

Conclusions: According to the results of the present study, it was concluded that in that AGA androgens lead to oxidative stress by increasing free oxygen radicals, which accelerates hair loss by causing microinflammation and fibrosis. The recognition of the effect of androgens and associated factors on the hair follicle cycle is essential for the development of new and effective treatment methods.

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Source
http://dx.doi.org/10.1111/jocd.13732DOI Listing

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