Background Allergic contact dermatitis is influenced by demographic factors. Updated epidemiologic data are needed to optimise patch test panels and preventive strategies.Objectives To evaluate trends and determinants of allergen sensitization in Korean patients undergoing patch testing.Methods Retrospective analysis of patch test records of 2271 patients at 15 university hospitals in Korea between 2019 and 2024. Patch test reactions were interpreted according to International Contact Dermatitis Research Group criteria. Association with age, sex, and body site was assessed.Results Overall, 57.1% of patients exhibited at least one positive reaction; among patients with positive reactions, 48.7% exhibited multi-sensitizations. Most frequent positive patch reactions were to nickel (29.0%), cobalt (18.2%), and chromium (8.2%). Women were more frequently sensitised to nickel and cobalt. Sensitization to fragrance mix I, Myroxylon pereirae resin, and p-phenylenediamine increased with age, whereas sensitization to thimerosal decreased. Facial involvement was associated with higher sensitization to lanolin alcohol; hand involvement with 2-mercaptobenzothiazole, colophonium, 4-tert-butylphenol formaldehyde resin and thimerosal; and scalp involvement with mercapto mix, 4-tert-butylphenol formaldehyde resin, p-phenylenediamine, and lanolin alcohol.Conclusions Metals, particularly nickel and cobalt, remain the predominant sensitizers in Korea. Age, sex, and localization differences underscore the need for targeted screening and public health strategies.

BACKGROUND:Rosacea is a chronic inflammatory skin disorder characterized by erythema, papules, ocular symptoms, and heightened sensitivity. Patients with neurogenic symptoms such as burning or stinging remain particularly difficult to manage. Current guidelines often underrepresent energy-based devices (EBDs), pigmentary sequelae, psychosocial burden, and ocular comorbidities. OBJECTIVE:To examine Korean dermatologists' expert perspectives on rosacea management, focusing on skin sensitivity, neurogenic symptoms, pigmentary changes, psychosocial impact, ocular involvement, and EBD use. METHODS:A web-based, 29-item survey was administered to 25 board-certified Korean dermatologists (May-June 2025). Quantitative and qualitative responses were analyzed. RESULTS:Erythematotelangiectatic and papulopustular phenotypes with sensitivity skin predominated. EBDs (pulsed dye laser, intense pulsed light) were frequently used but limited by cost and sensitivity issues. Neurogenic symptoms were recognized but rarely treated with neuromodulators. Post-inflammatory hyperpigmentation was infrequent, yet monitoring was inconsistent. Psychosocial and ocular aspects were acknowledged but seldomly systematically addressed. Respondents expressed interest in emerging adjunctive treatments such as cold plasma, skin boosters, and holistic care approaches. CONCLUSION:Korean dermatologists adopt individualized strategies for rosacea, yet practice gaps remain regarding neurogenic symptoms, pigmentary complications, and psychosocial and ocular comorbidities. Findings support the need for updated multidisciplinary, phenotype-driven guidelines aligned with real-world practice.

Pediatric atopic dermatitis (AD) shows distinct clinical characteristics compared to adult AD, suggesting unique inflammatory profiles that may influence disease prognosis and treatment response. We aimed to identify unique immune signatures of pediatric AD and investigate the differences between pediatric and adult AD patients. Nine pediatric (6-16 years) and 12 adult (20-60 years) were enrolled. PBMCs were collected from AD patients and age- and sex-matched healthy controls (HCs). Transcriptomic profiles were analyzed using single-cell RNA sequencing, and the immune phenotypes of adult and pediatric AD were compared. Th2 gene expression was elevated in both adult and pediatric AD, while Th1, Th17, and Th22 gene expression was downregulated in pediatric AD but not in adults. Genes involved in JAK/STAT signaling pathway, which were upregulated in adult AD, were not significantly increased in pediatric AD. The CD6-activated leukocyte cell adhesion molecule (ALCAM) pathway was upregulated in pediatric AD compared to pediatric HCs, but not in adult AD. Pediatric AD reveals distinct immune signatures, including a lack of JAK/STAT pathway upregulation observed in adult AD and a unique activation of the CD6-ALCAM pathway. These findings highlight the importance of age-specific treatment strategies in AD patients.

BACKGROUND:Atopic dermatitis (AD) is a common skin disease with a wide range of symptoms. Due to the rapidly changing treatment landscape, regular updates to clinical guidelines are needed. OBJECTIVE:This study aimed to update the guidelines for the treatment of AD to reflect recent therapeutic advances and evidence-based practices. METHODS:The Patient characteristics, type of Intervention, Control, and Outcome framework was used to determine 48 questions related to AD management. Evidence was graded, recommendations were determined, and, after 2 voting rounds among the Korean Atopic Dermatitis Association (KADA) council members, consensus was achieved. RESULTS:The guidelines provide detailed recommendations on foundational therapies, including the use of moisturizers, cleansing and bathing practices, allergen avoidance, and patient education. Guidance on topical therapies, such as topical corticosteroids and calcineurin inhibitors, is also provided to help manage inflammation and maintain skin barrier function in patients with AD. Additionally, recommendations on conventional systemic therapies, including corticosteroids, cyclosporine, and methotrexate, are provided for managing moderate to severe AD. CONCLUSION:KADA's updated AD guidelines offer clinicians evidence-based strategies focused on basic therapies, topical therapies, and conventional systemic therapies, equipping them to enhance quality of care and improve patient outcomes in AD management.

Ultraviolet radiation (UVR) is the most detrimental external factor that induces acute photodamage, photoaging and skin cancers, with complex underlying molecular mechanisms initiated mainly by increased DNA damage and reactive oxygen species (ROS) generation. Mitochondria are the main organelles in skin cells that produce ROS and energy and regulate various physiological and pathological signalling pathways. Continuous UVR on human skin can induce mitochondrial DNA mutations and excessive ROS production, creating feedback between each other and subsequently causing a reduction in mitochondrial membrane potential (MMP) and respiratory capacity. Deficiencies in mitochondrial function can induce apoptosis, mitophagy and senescence, resulting in UVR-induced skin photodamage and photoaging. Mitochondrial biogenesis and metabolic pathways play critical roles in the progression of skin cancers, particularly melanoma, which is the most malignant and infrequent type of cancer. In this review, we describe the recent advances in determining the intimate relationship between mitochondrial function and UVR-induced skin damage, suggesting potential molecular candidates and novel chemical/natural components to protect the skin from photoaging and skin cancers via mitochondrial targeting mechanisms.

While the starfish species Asterias pectinifera (Ap) and Asterias amurensis (Aa) are considered ecological threats to marine environments and the fishing industry, recent studies have identified them as rich sources of highly water-soluble, non-toxic collagen peptides. Mitochondrial dysfunction is a key driver of cellular senescence and skin aging, yet the therapeutic potential of marine-derived extracts in modulating mitophagy remains largely unexplored. In this study, we investigated whether starfish-derived extracts could mitigate senescence-associated phenotypes in human dermal fibroblasts (HDFs) through the modulation of mitophagy. Treatment with Ap- or Aa-derived extracts led to reduced senescence-associated β-galactosidase (SA-β-gal) activity, decreased expression of matrix metalloproteinase-1 (MMP-1), and suppression of pro-inflammatory cytokines including interleukin-6 (IL-6) and interleukin-8 (IL-8). Ap- or Aa-derived extracts significantly increased mitophagy in HDFs stably expressing mitochondrial-targeted Keima (HDF-mtKeima), while knockdown of PINK1, the essential regulator of mitophagy, abolished the mitophagy-inducing effects of Ap- or Aa-treatment, indicating that Ap- or Aa-derived extracts activate PINK1/Parkin-dependent mitophagy pathways. Importantly, PINK1 knockdown reversed starfish-induced suppression of MMP-1 and p21, demonstrating its crucial role in regulating senescence-associated gene expression. Additionally, Ap or Aa treatments significantly reduced reactive oxygen species (ROS) accumulation, improved mitochondrial function, and enhanced both basal and maximal respiratory capacity in senescent HDFs. These findings highlight that extracts derived from starfish promote mitophagy through PINK1-dependent mechanisms, exhibiting significant anti-senescence effects in HDFs. This suggests their potential application in the development of novel cosmeceuticals with skin-protective and rejuvenating properties.

Chitinase-3-like protein 1 (Chi3l1) is a member of the mammalian Chitinase-like protein family, and several studies reported that Chi3l1 is associated with various inflammatory diseases as well as liver diseases. Acetaminophen (APAP) is usually used for antipyretic drug, but its overdose induces acute liver injury (ALI). Several studies reported that subsequent inflammatory responses of the immune system play a critical role in the severity and outcome of APAP-induced ALI. In the present study, we investigated the role of Chi3l1 and its mechanism during APAP-induced ALI using Chi3l1 knock-out (KO) mice. We explored the function of Chi3l1 using APAP-injected KO mice and sought proteins associated with Chi3l1 through biological research data program for investigating mechanism. Liver histological analysis revealed that APAP-induced ALI was attenuated in KO mice compared to wild-type (WT) mice. We observed that APAP-induced neutrophil infiltration was decreased in the liver of KO mice compared to WT mice. To investigate this mechanism, we sought proteins potentially associated with Chi3l1 by mRNA sequencing and protein correlation analysis data. We found lipocalin-2 (Lcn2) and examined Chi3l1, Lcn2, and their relationship in the APAP-induced ALI model using recombinant proteins and antibodies. Our results suggest that Chi3l1 deficiency ameliorates APAP-induced liver injury through abrogating Lcn2-mediated neutrophil infiltration in the liver.

Brain aging is characterized by progressive structural and functional deterioration, leading to cognitive decline and impaired social functioning. A key factor in this process is the age-related decline in adult neurogenesis, particularly in the hippocampal dentate gyrus, which is linked to deficits in learning, memory, and increased social anxiety. Oxytocin, a neuropeptide synthesized in the hypothalamus, regulates social behavior, cognition, and emotion by acting on brain regions including the hippocampus. Importantly, oxytocin levels decrease with age, potentially contributing to cognitive impairment. Here, we examined whether chronic intraperitoneal oxytocin administration could attenuate cognitive decline in aged mice. Twelve-month-old mice received oxytocin injections (0.5 mg/kg) five times weekly for 13 weeks. Behavioral testing at 12 weeks of treatment using the object-place recognition task showed enhanced spatial learning and recognition memory in oxytocin-treated mice compared with saline controls. Immunohistochemistry revealed significantly increased doublecortin (DCX)-positive cells in the hippocampus, indicating enhanced neurogenesis. Furthermore, oxytocin treatment upregulated the expression of glutamate receptor 1 (GluR1) and N-methyl-D-aspartate receptor subunit 2B (NMDAR2B), which are markers of synaptic plasticity. These findings suggest that chronic oxytocin treatment is associated with enhanced neurogenesis and synaptic plasticity, which may contribute to improved cognition in aged mice. Our results support oxytocin as a potential therapeutic agent for age-related cognitive decline.