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This study identifies KLK14 as a significant factor contributing to hair defects and skin inflammation in a mouse model of Netherton syndrome.

This study found that recombinant murine IL-36α increased the number of regenerated hair follicles and accelerated wound healing in a mouse model of wound-induced hair follicle neogenesis.

This study found that specific gene upregulations and mutations in hidradenitis suppurativa skin support the role of inflammation, altered epithelial differentiation, and metabolism dysregulation in the disease's pathogenesis.

This study highlights the genetic complexities in alopecia areata, emphasizing the role of microRNAs and their association with other immune-related diseases, which could inform targeted treatment strategies.

In this review, the authors explore strategies for inducing scarless skin regeneration by modulating dermal signaling or specific fibroblast subsets to promote the formation of new hair follicles in wounds, particularly focusing on mimicking neonatal skin's regenerative capabilities.

Ixekizumab effectively treats generalized pustular psoriasis.

This review explores the role of neutrophil recruitment in the inflammation seen in hidradenitis suppurativa and emphasizes potential therapeutic targets within these pathways, but it reports no new clinical results.

This research observed that removing RNase L in mice enhances regenerative capacity through increased IL-36 and wound-induced hair neogenesis, highlighting RNase L as a gene that represses regeneration by moderating immune responses during viral infections.

This study found that dimethyl fumarate improved delayed wound healing in Il36rn-/- mice by reducing neutrophil extracellular trap formation and oxidative stress.

This review discusses the role of keratinocytes in hidradenitis suppurativa, highlighting their genetic and metabolic influences on disease progression without presenting new clinical results.

This study observed that mice treated with mrIL-36α showed differences in wound-induced hair neogenesis compared to those treated with PBS, indicating a potential role of mrIL-36α in hair growth after skin injury.

This study identified key genes and signaling pathways involved in the growth phases of Pashmina goat hair follicles, highlighting the role of several gene families and transcription factors in fiber quality and growth regulation.

2011 dermatological research found new skin aging markers, hair loss causes, skin defense mechanisms, and potential for new treatments.

This study reports that 71% of patients treated with the gamma-secretase inhibitor PF-03084014 for desmoid tumors experienced dermatologic side effects, such as follicular lesions and pruritic eruptions, which were managed with topical or systemic treatments.

This review discusses various nanoparticles and nanoemulsions being investigated for transdermal drug delivery and reports no clinical results; it highlights potential applications in treating alopecia, wound healing, psoriasis, and melanoma.

In this study, researchers found that cytokine dysregulation linked to genetic background is present in both patients and healthy but genetically related individuals in two autoimmune skin diseases, Pemphigus vulgaris and Alopecia areata, suggesting that protective immune mechanisms may prevent disease manifestation in predisposed individuals.

In this clinical trial, patients with lichen planopilaris treated with the oral TYK2 inhibitor deucravacitinib showed significant improvement in PGA, LPPAI, and Skindex-16 scores over 24 weeks, with transcriptomic analyses indicating decreased inflammatory and immune pathway activity post-treatment.

RNase L suppresses regeneration in mammals.

This study reported that the absence of Lsh in skin led to significant epidermal hyperplasia and altered gene expression, suggesting its crucial role in regulating epidermal proliferation, differentiation, and wound healing.

This review discusses the diagnosis and management of severe cutaneous adverse reactions to drugs and provides guidance for physicians to improve patient outcomes, but it reports no new clinical results.

This study identified changes in transcription factor gene expression across various signaling pathways during inner ear hair cell regeneration in birds, revealing patterns and potential new pathways for future investigation.

This review discusses the complex causes and treatment challenges of chronic inflammatory skin diseases, emphasizing the need for biomarkers to predict treatment responses; it reports no new clinical results.

In this study using genetic mouse models, researchers discovered that senescent melanocytes in nevi secrete osteopontin, which activates hair stem cells, enhancing hair growth; this process is mirrored in human hairy nevi, suggesting a potential therapeutic target for regenerative disorders.

This study identified upregulation of genes linked to fibroproliferative disorders, such as platelet-derived growth factor and collagen genes, in patients with central centrifugal cicatricial alopecia, suggesting potential therapeutic targets.

This study found that non-ablative fractional erbium glass laser treatment affected gene regulation in human skin models by downregulating MMP and interleukin expression, suggesting potential roles in dermal remodeling and anti-inflammatory effects.

This article reviews the roles of lesser-known secreted phospholipase A2 isoforms in various biological processes, such as immune suppression, metabolic regulation, epidermal hyperplasia, and male reproduction, without reporting new clinical findings.

This study found significant differences in gene expression between newborn and adult skin, with infant skin notably increasing processes related to ECM organization, cell adhesion, and collagen fibril organization.

This review discusses the application and potential of baricitinib, a JAK1/2 inhibitor, for treating dermatological diseases like alopecia areata and reports no new clinical results.

This study constructed a panel of pharmacokinetic and pharmacodynamic genes, revealing that current SNP chips insufficiently capture many drug-response gene variants, highlighting the need for complementary genetic approaches.