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This study observed that Trps1 gene expression in mice is precisely regulated in skin development, particularly during hair follicle morphogenesis, with distinct localization patterns in different cell types.

This review discusses recent insights into Birt–Hogg–Dube syndrome, including the functions of the FLCN gene and clinical recommendations for screening and treatment, but it reports no new experimental results.

This study suggests that changes in expressed transcripts and splice isoforms may explain the transition from curly to straight fleece in Chinese Tan sheep as they age.

This study found that in mice, EGFR activation suppresses mitotic regulators like Rcc2 and Stathmin 1, facilitating the transition to catagen in hair follicles.

The Fas/FasL pathway may play a role in alopecia areata.

This study identifies unique gene expression patterns in specialized fibroblasts within adult hair follicles, which advances understanding of their role in tissue regeneration.

This study found that Eda and activin A regulate Foxi3 expression, which may contribute to the development of hypohidrotic ectodermal dysplasia by affecting Foxi3 activity in ectodermal appendages like hair and teeth.

This study sequenced a related gene to KRT2.9 called KRT2.13, which encodes a type II keratin protein not expressed in the hair follicle, and found significant sequence homology suggesting possible gene conversion or conservation of functional sequences.

This study observed that adipose-derived stem cells modified with trichogenic factors have similar properties to dermal papilla cells and show enhanced hair regeneration potential compared to unmodified adipose-derived stem cells.

This report describes a boy with ectodermal dysplasias who was genetically diagnosed due to newly discovered TSPEAR gene variants, which have now been associated with this condition.

In this study, FGF5-knockout Dorper sheep generated using CRISPR/Cas9 showed increased fine-wool and active hair-follicle density, suggesting potential therapeutic applications for androgen alopecia.

This review discusses the role of Edar signaling in hair follicle development and cycling, emphasizing its impact on cell fate, differentiation, and interactions with other pathways, but reports no new results.

This review discusses the acyl-CoA synthetase very-long-chain (ACSVL) enzyme family, including its biochemical characteristics, tissue expression, and involvement in lipid metabolism, but presents no new experimental results.

The researchers in this study identified molecular mechanisms involved in frontal fibrosis alopecia, highlighting immune response and fatty acid metabolism, and developed a four-gene diagnostic model showing high accuracy in distinguishing affected individuals from controls.

In this study, researchers found that the deletion of Tet2/3 enzymes in mice led to changes in skin development and hair follicle differentiation, ultimately causing hair loss and altered gene expression.

This study concluded that KLF4 is a crucial regulator of hair follicle stem cell quiescence and may work by interacting with multiple transcription factors to control related genes.

This study reported that EGFR activation leads to suppression of Stathmin, which may promote synchronized entry into catagen in hair follicles, highlighting potential mechanisms involving EGFR in hair cycle transitions.

This article reviews the characteristics and inheritance patterns of keratosis follicularis spinulosa decalvans, but it does not present new clinical findings, noting the disease's complex and poorly understood pathogenesis.

In this study, researchers found that FGF9 plays a significant role in sheep wool growth by accelerating the proliferation and cell cycle of dermal papilla cells, potentially through regulation of the Wnt/β-catenin signaling pathway.

This article reviews the roles of several signaling pathways and molecules, including FGFs, Hh, Notch, TGF, and Wnt, in the development of teeth and hair follicles, but reports no new findings.

This study suggests that TGF-β 2 plays a critical role in hair follicle morphogenesis and may enhance the effectiveness of future cell therapies for hair regrowth using expanded dermal papilla cells.

The Dfl mutation in mice causes poor sebaceous gland function and complete hair loss.

This study observed that antisense oligonucleotides targeting FGFR-1 increased cellular activity in hair follicle cultures from mice, suggesting potential clinical utility for treating baldness.

In this study, deleting the transcriptional pause factor Nelfb in mouse preadipocyte lineages led to defective dermal fat formation and lethal outcomes, while interventions targeting Pparg could rescue adipocyte differentiation and promote dermal white adipose tissue formation, underscoring Nelfb's critical role in adipogenesis.

This study found that TLR2 expression in hair follicle stem cells is crucial for hair follicle maintenance and regeneration, with TLR2-dependent activation potentially offering new therapeutic approaches for hair loss prevention through mechanisms involving immune pathways and CEP administration.

This study identified a heterozygous de novo mutation in the ODC1 gene causing a new disorder characterized by overgrowth and developmental delay, and suggests that DFMO treatment may help manage elevated ODC activity and putrescine levels.

This study found that exogenous EGF inhibited hair follicle development and decreased follicle density in both Tabby and normal mice, suggesting interactions between EGF and the Ta peptide influence normal skin phenotype.

This study observed distinct differences in hair characteristics between individuals with cardio-facio-cutaneous syndrome and Costello syndrome, highlighting the role of the RAS pathway in these RASopathies and aiding clinical diagnosis.

In this open-label trial, Tofacitinib was well tolerated and improved IFN and cytokine scores, as well as overall skin pathology, in individuals with Down syndrome and immune skin conditions.

Folliculin slows hair growth, and blocking it might help treat hair loss.