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IL-6 contributes to hair loss by shortening the growth phase and causing hair follicles to regress.

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.

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.

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 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.

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 the microRNA miR-22 is a key regulator of the hair cycle, influencing hair loss by promoting the transition from growth to rest phases and repressing keratinocyte differentiation.

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 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.

This study found that endothelin produced by hair follicle progenitors activates contractions in dermal sheath cells, facilitating hair follicle regression in the growth cycle.

This study suggests that policosanol may prevent androgenetic alopecia in mice by regulating hormone levels and suppressing premature hair follicle entry into the regression phase.

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 found that targeting connective tissue sheath contraction with an MLCK inhibitor may improve hair growth in androgenetic alopecia by reducing premature hair regression caused by ectopic apoptosis of hair follicle progenitor cells.

In this study using live mice, researchers observed that during hair follicle regression, apoptosis in basal cells may propagate by triggering neighboring cells, potentially regulated by a gradient of pro-survival signals from stem cells, and proposed a testable mechanism to further explore this process.

This study found that the dermal sheath smooth muscle regulates hair follicle progenitor cell death during hair regression through mechanical signaling of the TGF-β pathway.

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 in live mice suggests that hair follicle regression involves apoptosis propagation towards stem cells, potentially slowed by a protective signal from the stem cells themselves.

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 identified TGF-β2 as a crucial signal in hair follicle stem cell regeneration, highlighting its role in counteracting BMP signaling to promote tissue regeneration.

This study found that increased MSI2 expression in hair follicle stem cells can delay hair growth by maintaining stem cell quiescence and repressing Hedgehog signaling.

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.

Stress can cause hair loss and skin issues by affecting hair growth cycles.

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 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 review explores the molecular processes behind hair follicle stem cell activation and suggests new potential targets for designing therapies for various types of alopecia, but it reports no clinical results.

The researchers reported that Gambogic Amide may prevent hair greying and promote hair growth by maintaining follicle pigmentation in vitro through activation and migration of melanocytes.

Caspase-7 has functions in skin and hair that are not related to cell death.

This study identified the dermal sheath as a driver of hair follicle regression through muscle contraction, essential for reuniting niches and stem cells to regenerate tissue structure during homeostasis.

This study found that miRNA biogenesis, facilitated by Dicer and Drosha, is crucial for adult hair follicles' growth and regeneration, highlighting their multiple roles during the hair follicle growth cycle.