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This study found that selenium deficiency in mice accelerated age-related conditions and metabolic decline but unexpectedly promoted longevity, suggesting low selenium levels might separate healthspan and lifespan.

In this study, knockout mice lacking the Cyp4f39 gene showed severe skin barrier dysfunction and high early mortality, suggesting its critical role in skin barrier formation and insights into ichthyosis pathogenesis.

This study suggests that in gp91phox-knockout mice, tranexamic acid administration led to brown hair by increasing MGRN1 and collagen XVII levels, while the retention of black hair appears to rely on the gp91phox/ROS/IL-1β/TGF-β pathway.

This study reported that a novel cationic liposome formulation for delivering encapsulated Cas9 protein and sgRNA successfully decreased SRD5α2 mRNA expression by 29.7% in vitro, suggesting a potential alternative treatment option for conditions like prostate cancer and benign prostatic hyperplasia without current drug side effects.

This study generated FGF5-knockout Dorper sheep using the CRISPR/Cas9 system, resulting in significantly increased fine-wool and active hair-follicle density, and explored downstream signaling pathways for potential applications in androgen alopecia treatment.

In this study, researchers identified a new dominant mutation in Hairless mice, called Pied, resulting from a deletion in the Adam10 gene, which causes freckle-like skin pigmentation by inhibiting melanocyte expansion.

This study found that K17 is crucial for the structural integrity and survival of hair-producing cells, with K17 null mice developing alopecia due to hair fragility and follicular alterations.

This study observed that deleting PTEN in mouse facial motoneurons enhanced peripheral axon regeneration but also led to physiological changes and potential hyperplasia in older mice.

In this study, a high-fat, high-cholesterol diet in atherosclerotic mice led to skin inflammation and hair problems, which could be reversed by inhibiting glycosphingolipid synthesis.

In this study, researchers found that Fgf21 knockout mice exhibited delayed hair follicle cycling compared to wild-type mice, potentially due to altered miRNA interactions affecting Vezf1 and Map3k1 expression, providing insights into the molecular regulation of hair growth.

In this study, a low-methionine diet significantly improved the health and physical traits of cystathionine β-synthase-deficient mice, contrasting with negative effects on mice with partial deficiency.

This study observed that disrupting the Pnkp gene in adult mice resulted in a premature aging-like phenotype, suggesting PNKP's vital role in maintaining normal growth and survival of certain progenitor cell populations.

In this study, DHT was found to inhibit hair growth in mice by decreasing IGF-I production in dermal papillae through reduced sensory neuron stimulation.

Eating isoflavone can help mice grow hair by increasing a growth factor.

This study observed that transgenic mice with overexpression of HE4 developed keratitis and severe corneal opacity, suggesting that HE4 may significantly influence keratopathy and inflammatory responses in the eye.

This study highlights the potential of GPR30 and its selective agonists as promising therapeutic targets for treating hair loss disorders and conditions that respond to estrogen, emphasizing their role in modulating hair growth.

PTHrP is important for bone formation and may be targeted for osteoporosis treatment and longevity therapies.

This study found that deleting the ATR gene in adult mice led to rapid onset of age-related traits such as hair graying and osteoporosis through reduced regenerative capacity.

This study found that mutant mice with the we/we wal/wal genotype exhibit significant defects in hair shaft structure and epidermis stratification, correlating with postnatal alopecia symptoms.

This study used developing mouse hair follicles to explore early epithelial bud formation, finding that the Rho GTPase regulator ARHGEF3 plays a crucial role in regulating cell fate and cadherin patterning, with knockouts showing disrupted morphology and increased straight hair follicle growth.

This study found that transient mtDNA double strand breaks in mice accelerated aging in certain tissues through increased reactive oxygen species, independent of p21/p53 pathway mediation.

This study found that prolonged Nrf2 activation in mouse keratinocytes led to enlarged sebaceous glands, hair loss, and cysts, suggesting a role for Nrf2 in conditions like MADISH.

This study found that epidermal melanocytes can regenerate hair follicles, whereas non-cutaneous or dermal melanocytes cannot, suggesting two distinct melanocyte lineages with potential implications for melanocyte-related diseases.

This review discusses dietary manipulation strategies in a mouse model of CBS deficiency and reports no new results; the authors emphasize the importance of understanding gene-diet interactions.

This research suggests that targeting the HIF-1α pathway via PHD inhibitors may enable regeneration similar to amphibians in mammals, potentially fast-tracking regenerative therapies from mice to humans.

In this study, Trapa bispinosa Roxb. pericarp extract demonstrated inhibitory effects on 5α-reductase activity both in vitro using LNCaP cells and in vivo in a mouse model of benign prostatic hyperplasia, suggesting its potential role in managing the condition.

In a conditional knockout mouse model, this study found that loss of the transcription elongation factor SPT6 in basal keratinocytes led to psoriasis-like skin inflammation and delayed wound healing, suggesting SPT6 plays a crucial role in maintaining epidermal immune quiescence by suppressing proinflammatory NF-κB signaling.

This study found that Wnt secretion is important for maintaining skin homeostasis in mice, as Evi-deficient mice developed psoriasis-like skin lesions and had an imbalance in immune cell populations.

This study found that mitochondrial fusion regulator Opa1 is crucial for maintaining melanocyte stem cells during the hair follicle cycle in mice, with Opa1 deficiency leading to impaired SCF-KIT signaling, reduced melanocyte populations, and early hair graying.

This study used Cisd2 knockout mice models and found that these mice display premature aging characteristics and an increase in dysfunctional neutrophils, suggesting Cisd2's role in calcium homeostasis and neutrophil function via interactions with Calnexin and SERCA.