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This study found that dual inhibition of BACE1 and BACE2 in mice affects melanosome maturation and causes dose-dependent hair depigmentation without altering retinal morphology.

This study found that finasteride treatment improved cardiac function and reduced heart failure progression in mice, suggesting it could be a potential therapy for pathological cardiac hypertrophy and dysfunction.

In this study, mouse sweat gland development relied on a regulatory sequence initiated by Wnt/β-catenin signaling, and disruptions in Wnt, Eda, or Shh pathways led to distinct developmental failures.

This study found that FOXN1 haploinsufficiency is a significant genetic factor causing T cell lymphopenia at birth, linked to reduced thymic function in both humans and mice.

In this study, ectopic Wnt10b-mediated β-catenin activation in hair follicles resulted in larger regenerating anagen hair structures, an effect modulated by the Wnt inhibitor DKK1.

The study found that severe insulin resistance and premature diabetes are common in patients with PCNT genetic defects, primarily affecting those over four years old, while not impacting early insulin signaling in adipocytes.

This review presents updated tables of mouse mutants with hair growth abnormalities to aid in understanding the molecular mechanisms of human hair disorders, but reports no new clinical results.

This study found that the antiandrogen drug enzalutamide reduced TMPRSS2 levels and significantly decreased SARS-CoV-2 entry and infection in lung cells, supporting further clinical trials for COVID-19 treatment.

In this study, decreased expression of BMP2 and ephrin A3 and increased NT-4 gene expression were observed in dermal papilla cells from androgenic alopecia-affected skin, suggesting potential roles in hair growth regulation.

This study found that a 3D Matrigel culture technique for dermal papilla cell spheroids can enhance hair follicle inductivity and induce hair-like fiber differentiation in vitro, even with high-passage cells.

This study identified hair shaft progenitors in the matrix that regulate hair growth and pigmentation by creating a niche dependent on stem cell factor, implicating KROX20+ cells in these processes.

This study observed that Ptprq mutant mice exhibit significant abnormalities in hair bundle structure and vestibular dysfunction, suggesting similar issues may contribute to hearing loss and vestibular problems in humans with PTPRQ mutations.

This study found that specific mutations in the spike protein of SARS-CoV-2 may significantly alter its structure and affect how it binds to certain inhibitors, but experimental studies are needed to confirm potential clinical implications.

This study found that lymphatic vessels in mice are important for hair follicle development and organization, as their depletion blocks hair growth.

This article updates a diagnostic tool (SALT II) for assessing hair loss by adding more precise measurements of scalp surface area, particularly useful for various types of alopecia.

This study suggests that women with polycystic ovary syndrome may have a distinct metabolomic profile, differing in levels of amino acids, organic acids, and lipids compared to controls.

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.

This chapter reviews surface plasmon resonance (SPR) methodology and its applications in basic science and human disease without reporting new clinical results.

This review explores the novel roles of white adipose tissue in tissue homeostasis and regeneration, emphasizing its impact on epithelial, muscle, and immune tissues, and reports no new clinical results.

This study suggests that heparan sulfate is crucial for regulating hair follicle formation, cycling, and gland morphogenesis, with its ablation leading to continuous hair growth and increased gland activity in mice.

This study revealed that deficiency in the enzyme FA2H in mice affected sebaceous gland function, altered sebum composition, and caused cycling alopecia, highlighting FA2H's role in hair follicle homeostasis.

The researchers reported that in mice, prolactin signaling in the skin epithelium inhibits hair follicle stem cell activation, promoting quiescence during periods of high serum prolactin like pregnancy and lactation.

This review presents standardized methods for assessing and tracking hair loss in alopecia areata but reports no clinical results, with the authors noting time limitations in clinical practice.

This study used proteomic techniques to analyze human hair proteins, revealing keratin heterogeneity and identifying posttranslational modifications, such as cysteine trioxidation and methylation.

This study found that platelet-derived growth factor signaling is crucial for maintaining the hair follicle dermal stem cell pool and supporting their regenerative capacity.

This study demonstrated that keratin derived from human hair can improve axon extension and alleviate motor deficits from sciatic nerve injuries, highlighting its potential as a promising biomaterial for peripheral nerve regeneration.

This study found that sweat gland stem cells primarily maintain sweat gland homeostasis but can trans-differentiate to aid in epidermal healing and regenerate diverse skin structures under certain conditions.

This study observed that dietary intake of glucoraphanin during juvenile and adolescent stages prevented cognitive deficits and abnormal gene expressions in the brain of adult offspring exposed to maternal immune activation, potentially implicating centrosome-related genes in the development of psychosis.

This study found that the dermal papilla of the hair follicle regulates stem cell quiescence and regeneration by modulating Shh and Wnt signaling pathways, highlighting the importance of signaling cross talk in regeneration.

This study reports that hypomorphic alleles of the Ass1 gene in mice resemble human CTLN1, providing a potential model for preclinical studies and indicating that standard treatments for CTLN1 can rescue phenotypes.