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This study found that intradermal injection of cholesterol-modified siRNA targeting FGF5 or FGF18, or topical application of FGF18-targeted siRNA, effectively influenced hair follicle cycles in mice, suggesting potential benefits for alopecia management.

In this study, researchers found that both direct and witnessed trauma in mice are associated with reduced levels of the neurosteroid allopregnanolone, potentially influencing PTSD outcomes, and that treatment with synthetic neurosteroids may mitigate fear responses linked to observed trauma.

This study found that mature dermal adipocytes have high plasticity, undergoing dedifferentiation and redifferentiation, which plays a significant role in hair cycling and wound healing.

This study found that knocking out the Hars2 gene in mouse cochlear hair cells led to mitochondrial dysfunction and ROS stress, resulting in progressive hearing loss and differential effects on inner and outer hair cells.

This study revealed that Vav2 and Vav3 play roles in regulating hair follicle bulge stem cells in normal conditions and cancer stem cell activation and remodeling in mice.

In this study, activation of Tgr5 was found to improve alopecia areata and bone microstructure in mice by down-regulating the JAK1-STAT3 signaling pathway.

This study found that MPZL3 knockout mice showed reduced dermal white adipose tissue and increased sebocyte proliferation, suggesting a regulatory role for MPZL3 in lipid metabolism balance between adipocytes and sebocytes.

This study provides genetic evidence that desmoglein-1 can compensate for the loss of desmoglein-3 in hair adhesion, supporting the desmoglein compensation hypothesis.

This study observed that vitamin D receptor knockout mice exhibit impaired epidermal differentiation and progressive hair loss, suggesting the importance of the vitamin D receptor in normal skin and hair follicle development.

This study found that calbindin-D9k knockout mice on a maternal vitamin D-deficient and low-calcium diet developed transient alopecia, but a high-vitamin D and calcium diet in mothers reduced this effect.

This study found that deleting β-catenin in epidermis-specific VDR knockout mice did not prevent UVB-induced skin tumors, indicating β-catenin does not compensate for VDR's role in tumor suppression.

This study reports that the autotaxin–LPA–LPA3 signaling pathway at the embryo-epithelial boundary plays a critical role in decidualization by up-regulating HB-EGF and COX-2 in the uterine epithelium.

This study found that inhibiting AP-1 activity in mice can induce lineage transdifferentiation between squamous and sebaceous tumors, suggesting AP-1's role in maintaining tumor cell identity.

In a study on mice, researchers found that exposure to artificial light environments causing circadian misalignment impaired hair growth by reducing the hair growth rate during the anagen phase, suggesting these light conditions as a potential risk factor for hair loss.

In this study, inducible whole-body Acly-knockout mice revealed that ACLY is essential for skin homeostasis, as its deficiency led to increased sebum production and skin abnormalities, indicating a vital role for cytosolic acetyl-CoA synthesis in preserving skin barrier integrity and systemic lipid regulation.

This publication provides a standardized nomenclature for classifying microscopic lesions in laboratory rat and mouse skin, aiming to harmonize international toxicological research.

This study found that the loss of Msx2 in knockout mice led to phenotypes similar to Peters anomaly and microphthalmia, suggesting that MSX2 plays a critical role in anterior segment development of the eye.

This article reviews sPLA2-mediated phospholipid metabolism using sPLA2 transgenic/knockout mice and lipid mass spectrometry, offering insights into the distinct roles of sPLA2 enzymes in various biological events.

This study found that deleting ceramide synthase 4 in skin epidermis stem cells disrupts hair follicle and skin barrier function, leading to immune responses similar to atopic dermatitis, due to imbalances in lipid composition affecting differentiation.

This review explores the immunological aspects of epidermal differentiation in loricrin knockout mice, offering insights into keratinization and potential intrinsic factors affecting immune function, but provides no new clinical findings.

This study found that overexpression of Gsdma3 in mice led to epidermal hyperplasia, skin inflammation, and hair growth defects, suggesting gain-of-function mutations in Gsdma3 cause these conditions.

This review discusses the role of YAP/TAZ proteins in skin cancer physiology and tumorigenesis, and the potential of targeting these proteins in skin cancer treatments, but presents no new experimental findings.

This study observed that deleting ARNT in keratinocytes of mice reduced zigzag hair production and altered hair follicle differentiation, likely by affecting the expression of specific cyclin-dependent kinase inhibitors.

This study found that inhibiting AP-1 transcription factors in mice causes squamous tumors to transform into sebaceous tumors and regulates tumor cell lineage.

This review discusses the state-of-the-art knowledge on pseudoxanthoma elasticum, summarizing recent advancements in genetics, pathomechanisms, and potential treatments but reports no new clinical findings.

This study found that adipose-derived stem cell-conditioned media improved skin flap survival following ischemia/reperfusion injury in mice by increasing cell proliferation and the number of hair follicles, mediated by IL-6.

This study suggests that dietary vitamin A may influence alopecia development and progression, but the mechanisms remain unclear, highlighting the interplay between genetics and nutrition in these hair loss conditions.

In this study, knockout of B-raf and C-raf genes in mice showed they are not needed for early melanocyte development, but are crucial for maintaining melanocyte stem cells, as evidenced by hair graying due to stem cell depletion.

In this review, extensive analysis using conditional mutant mice revealed that androgen and Wnt signals play crucial roles in the development and function of male external genitalia and erectile tissue, while also exploring various regulatory factors involved in their pathogenesis.

This review examines rodent models to explore how maternal conditions like undernutrition, obesity, hypoxia, and androgen exposure affect fetal programming and metabolic outcomes in offspring, but presents no new clinical findings.