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The study identified the retarded hair growth (rhg) mutation in mice as an allele of the ornithine aminotransferase (Oat) gene, caused by a G to C transversion in Exon 9, leading to a glycine to alanine substitution. This mutation resulted in elevated plasma ornithine levels, reduced OAT activity, and symptoms such as delayed hair growth, cataracts, and retinal degeneration, making it a potential model for human gyrate atrophy of the choroid and retina. The study involved a large backcross panel of 1,462 mice and 65 offspring from specific crosses, providing a robust model for understanding OAT deficiency. Arginine supplementation improved growth in mutant mice, supporting the link between the rhg mutation and OAT deficiency.

This study investigates the role of lipids in hair growth, particularly through the HIF-1 signaling pathway. Researchers observed reduced lipid metabolism in the scalp tissues of patients with androgenetic alopecia. Supplementing lipids in culture mediums enhanced hair growth-related gene expression and the proliferation of human dermal papilla cells (DPCs). RNA-sequencing and HIF-1a knockdown experiments identified HIF-1a as a key regulator in lipid-induced upregulation of trichogenic genes. Additionally, lipids were shown to promote the elongation of hair-shaft-like structures in vitro. These findings suggest that targeting lipid metabolism and HIF-1 signaling could be a promising approach for treating hair loss.

In this study, researchers created a transgenic mouse line that overexpressed spermidine/spermine N^1-acetyltransferase, leading to significant alterations in tissue polyamine pools. These changes included the presence of N^1-acetylspermidine, an unusual accumulation of putrescine, and reduced levels of spermidine and spermine. The most notable phenotypic effect was permanent hair loss in mice aged 3 to 4 weeks, associated with the formation of follicular cysts in the dermis, likely due to putrescine's interference with hair follicle cell differentiation and proliferation. Additionally, female mice were infertile, linked to ovarian hypofunction and underdeveloped uteri. This research highlighted the potential of using spermidine/spermine N^1-acetyltransferase overexpression to manipulate polyamine levels in transgenic animals for studying developmental and cancer-related outcomes.