Local Artemis dysfunction may be one molecular mechanism for androgenetic alopecia via telomere shortening

The article suggests that local Artemis dysfunction may be a molecular mechanism for androgenetic alopecia via telomere shortening. Androgenetic alopecia is the most common cause of hair loss related to dihydrotestosterone, characterized by progressive miniaturization and an increase in telogen ratio. Reduction in overall cell numbers, which may be the result of cell apoptosis or proliferation inhibition, is likely to account for the decrease in hair follicular size. The study shows that telomere shortening inhibits stem cell proliferation, resulting in immobilization of stem cells in their niche and hair follicle miniaturization. Artemis, a member of the SNM1/PSO2 gene family, has the ability to maintain telomere function and protect against multi-organ developmental failure. Recent studies show that telomere dysfunction phenotype can be caused by defective Artemis in human cell lines, and Artemis mutations have been detected in Omenn syndrome, which is associated with alopecia. Therefore, Artemis may be involved in hair growth via telomere maintaining.