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This study found that thrombospondin-1 plays a critical role in hair follicle cycle regulation, with deficiency prolonging follicle growth and overexpression delaying it through antiangiogenic effects.

This study found that applying dexamethasone to mice induced catagen-like follicle changes significantly earlier and more consistently than a vehicle, such changes being useful for studying hair follicle regression.

This study found that the retinoid all-trans retinoic acid induced a catagen-like stage in human scalp hair follicles, suggesting upregulation of TGF-beta2 as a contributing mechanism.

In this study, different types of catagen in the C57BL/6 mouse model exhibited varying effects on hair follicle melanocytes and melanin distribution, with spontaneous and dexamethasone-induced catagen showing pigment incontinence, while cyclophosphamide-induced catagen retained dendritic melanocytes but increased ectopic melanin.

This study observed that downregulation of laminin-511 plays an important role in hair regression during the catagen stage in mice.

This study found that numerous genes involved in hair growth, including 73 co-up-regulated ones, were differentially expressed in goat hair follicles during the hair growth cycle.

This study suggests that the expression of the DP2 receptor is higher in balding scalp cells and that its knockdown could inhibit the transition to the catagen phase in cultured human hair follicles, potentially counteracting hair growth inhibition associated with male pattern baldness.

This article explores the complexity and significance of the hair follicle, emphasizing new insights into its biological roles and the involvement of p53 in follicular regression.

This study found that the switch-off of melanogenesis during the hair cycle in C57 BL-6 mice is a gradual and stochastic process starting in mid anagen VI, with specific biochemical markers indicating the transition to catagen.

This study expands knowledge of non-coding RNAs in goats and other mammals, enhancing understanding of their roles in hair follicle growth and regression.

This study found that Gsdma3 mutation in mice allows hair follicles to bypass a typical telogen phase and directly enter the anagen phase, suggesting Gsdma3's role in hair cycle transitions by regulating Wnt signaling.

The study found that prolactin expressed in human scalp hair follicles acts as an autocrine modulator, inhibiting hair growth and promoting hair follicle regression, which may contribute to hair loss in hyper-prolactinemia patients.

In this study, researchers found that p75 neurotrophin receptor signaling affects apoptosis during hair follicle regression in mice, and altering its activity might help manage disorders involving early catagen entry.

This study found that p53 plays a crucial role in regulating apoptosis during hair follicle regression (catagen) in mice, and its absence leads to delayed progression and altered expression of apoptosis-related markers.

This study found that overexpressing human Bcl-2 in mice protected epidermal keratinocytes from UVB-induced apoptosis but unexpectedly increased apoptosis during hair follicle regression and chemotherapy.

This study found that ICAM-1 expression in murine skin is developmentally regulated and crucial for skin and hair follicle remodeling beyond its recognized role in immune responses.

In this study, a synthetic antagonist of the p75 neurotrophin receptor was found to significantly inhibit hair follicle regression in murine skin cultures, suggesting a potential role in treating hair disorders characterized by premature catagen entry.

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

In this study, researchers observed that Vdr-knockout mice experience hair cycle arrest during the catagen stage, leading to alopecia, with persistent epithelial strands forming in the hair follicles, indicating Vitamin D receptor's role in regulating hair follicle regression and regeneration.

This study suggests that the down-regulation of 14-3-3 proteins in wild-type keratinocytes, absent in Smad4 mutant keratinocytes, might contribute to the failure of hair follicles to initiate catagen in Smad4 knockout mice.

This study found that Bnip3L and caspase-12 were differentially expressed during the first catagen stage of mouse hair follicle development under normal physiological conditions.

This study identified the dermal sheath as a key component of the hair follicle niche, essential for outer root sheath regression during the hair cycle, highlighting its importance in hair follicle support and regulation.

This study found that the loss of a functional hr gene in mice leads to premature and abnormal hair follicle regression, disrupting normal hair cycling and architecture.

This study identified distinct gene expression patterns in wool follicle bulbs that may play important roles in wool follicle cycling and regeneration in sheep.

In this study, researchers used two dermal papilla spheroid models to investigate hair cycle regression mechanisms and found that the vascular system enhances tissue physiology and gene modulation, while Retinol-based treatments can partially recover tissue degeneration observed over an extended culture period.

This study found that infused mouse epidermal growth factor induced wool follicle involution through a quasi-physiological process similar to catagen and a separate pathological action, resulting in fleece 'break' or shedding.

This study found that deleting the miRNA processing enzymes Drosha and Dicer from mouse skin epithelial cells disrupted normal hair follicle development and maintenance, leading to follicular degradation and stem cell loss during the growth phase.

This study found that Polygonum multiflorum extract may promote hair growth by increasing anagen duration and activating dermal papilla cells in human hair follicles, as observed in cultured cell models.

This study found that lymphatic vessels promote hair follicle growth in mice, suggesting new therapeutic strategies for hair loss treatments.

This study found that keratin 17 and TNFα play interdependent roles in regulating hair follicle cycling, with TNFα required for the anagen–catagen transition and its ablation partially rescuing hair cycling defects in K17-null mice.