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This study demonstrated that a combination of four types of honey significantly improved hair integrity, porosity, and surface roughness after exposure to UV-A and pollution stress.

This study found that knockdown of PCAT1 inhibited hair follicle regeneration in nude mice by disrupting the miR-329/Wnt10b axis and Wnt/β-catenin signaling, highlighting PCAT1's role in promoting follicle regrowth.

This study found that the JMJD3/NF-κB-Notch1 pathway plays a crucial role in regulating keratinocyte migration and skin wound healing, with Notch1 affecting key genes involved in cell migration.

This study found that Wnt/β‐catenin signaling influences the hair follicle regeneration process by prompting quiescent stem cells to enter the cell cycle and is necessary for maintaining the stem cell pool.

This study found that Wnt signalling activates hair follicle fate in hair follicle stem cells by relieving TCF3/4–TLE-mediated repression, with β-catenin being crucial for this process.

In this study, in ovo injection of CHIR-99021 promoted the morphogenesis and development of feather follicles in chick embryos by activating the Wnt/β-catenin signaling pathway.

In this study, researchers found that transgenic expression of the Hairless gene in keratinocytes can restore hair follicle regeneration in Hr-deficient mice by repressing Wise, a modulator of Wnt signaling.

This study found that p21 is much more highly expressed in normal melanocytes compared to melanoma cells, suggesting a potential target for preventing melanoma progression through cell cycle repair processes.

This study investigated dermal fibroblasts in mouse skin using single-cell RNA sequencing and identified signaling pathways that influence adipogenesis, finding that IL-1-NF-κB promotes, while WNT-β-catenin inhibits, the adipogenic potential of these cells, with implications for wound healing and scar formation.

This study found that disrupting the inturned gene in developing mouse epidermis halted hair follicle formation due to impaired keratinocyte differentiation, highlighting primary cilia's role in tissue-specific planar cell polarity signaling.

This article discusses the advances in understanding wound-induced hair follicle neogenesis (WIHN) and highlights the roles of specific signaling pathways and cellular plasticity, noting no clinical results but suggesting potential areas for further research.

In this study, NB-UVB therapy significantly increased Wnt1 and β-catenin expression in hair follicles, which may play a role in vitiligo perifollicular repigmentation.

This review explores the cellular and molecular basis of wound-induced hair neogenesis and its relationship with aging but does not report new clinical results, highlighting areas for future research.

This study found that the Wnt-β-catenin pathway directly promotes TERT expression in both stem and cancer cells, highlighting a mechanistic link between tumorigenesis and pluripotency.

This study provides a detailed analysis of cell subpopulations in a mouse model of wound-induced hair follicle regeneration, revealing specific cellular dynamics and heterogeneity that may influence hair follicle neogenesis.

This study reported that in a mouse model, Negative Pressure Wound Therapy promotes wound healing by modulating inflammatory responses and increasing dickkopf-related protein 1, which encourages the differentiation of Hair Follicle Stem Cells into epidermal cells.

This study demonstrated that combining the Wnt/β-catenin activator CHIR99021 with 3D spheroid culture effectively enriched hair follicle formation in reconstituted human skin.

This study found that overexpressing the 14-3-3σ protein in transgenic mice reduced keratinocyte proliferation and migration, leading to thinner epidermis and fewer hair follicles due to IGF-1 pathway inhibition.

In this study, a mouse model with a PIK3CA gain-of-function mutation in Schwann cells revealed unique communication with neighboring cells and a glycolytic shift in peripheral nerves, and early alpelisib treatment significantly improved symptoms, though efficacy declined with delayed administration due to limited drug penetration.

This study found that treating wounds in mice with the drug verteporfin, which inhibits mechanical signaling, leads to skin regeneration associated with the activation of Wnt pathway proteins.

This study found that Basonuclin 1 knockdown in human primary keratinocytes significantly reduces cell proliferation and affects migration, indicating its role in coordinating the re-epithelization phase of wound healing.

This study found that Frizzled genes Fzd3 and Fzd6 are redundantly involved in controlling hair follicle polarity in mice, but operate through distinct mechanisms, highlighting their complex role in hair orientation.

This study found that SWI/SNF complexes, especially the ATPase BRG1, are crucial for keratinocyte migration in human wound healing but do not affect hair growth in short-term hair follicle cultures.

In this study on fine-wool sheep, researchers found that overexpressing the TGFBR1 gene decreased proliferation of dermal papilla cells by influencing multiple signaling pathways, suggesting TGFBR1 as a negative regulator in hair follicle development.

This study found that mice with a homozygous knockout of the Ten1 gene, developed through CRISPR-Cas9-mediated exon 3 deletion, exhibited telomere shortening and symptoms consistent with accelerated aging, such as reduced lifespan, skin changes, aplastic anemia, and cerebellar hypoplasia.

This review examines the Wnt signaling pathway's role in regeneration across key model species, but it reports no new findings and highlights the need for more research to understand the underlying molecular mechanisms.

This study found that inhibiting the interaction between HOTAIR and EZH2 can block pro-fibrotic gene expression in fibroblasts and interfere with tissue remodeling in systemic sclerosis patient skin.

This study found that WD-aptamer increased β-catenin expression and promoted human hair follicle dermal papilla cell proliferation by interfering with the CXXC5-Dvl1 interaction in the Wnt signaling pathway.