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The dermis is primarily composed of the extracellular matrix (ECM) and fibroblasts. During the aging process, the dermis undergoes significant changes. Collagen, which is a major component of ECM, becomes fragmented and coarsely distributed, and its total amount decreases. This is mainly due to increased activity of matrix metalloproteinases, and impaired transforming growth factor-β signaling induced by reactive oxygen species generated during aging. The reduction in the amount of collagen hinders the mechanical interaction between fibroblasts and the ECM, and consequently leads to the deterioration of fibroblast function and further decrease in the amount of dermal collagen. Other ECM components, including elastic fibers, glycosaminglycans (GAGs), and proteoglycans (PGs), also change during aging, ultimately leading to a reduction in the amount of functional components. Elastic fibers decrease in intrinsically aged skin, but accumulate abnormally in photoaged skin. The changes in the levels of GAGs and PGs are highly diverse, and previous studies have reported conflicting results. A reduction in the levels of functional dermal components results in the emergence of clinical aging features, such as wrinkles and reduced elasticity. Various antiaging approaches, including topicals, energy-based procedures, and dermal fillers, can restore the molecular features of dermal aging with clinical efficacy. This review summarizes the current understanding of skin aging at the molecular level, and associated treatments, to put some of the new antiaging technology that has emerged in this rapidly expanding field into molecular context.

Melasma is a commonly acquired hypermelanosis that affects sun-exposed areas of the skin, with frequent facial involvement. Its histologic manifestations are evident in the epidermis, extracellular matrix, and dermis. In addition to epidermal pigmentation, pathologic findings of melasma include extracellular matrix abnormality, especially solar elastosis. The disrupted basement membrane has been described in melasma with variable incidences. In the dermis, an increase in vascularity and an increase in the number of mast cells were observed, indicating that dermal factors have critical roles in the pathogenesis of melasma, despite the fact that melasma is characterized by epidermal hyperpigmentation. This review discusses such histologic characteristics of melasma, with consideration to their implications for melasma treatment.

To test the hypothesis that intrinsic renal scattered tubular cells (STC-like cells) contribute to repairing injured tubular epithelial cells (TEC) by releasing extracellular vesicle (EV). EV released from primary cultured pig STC-like cells were confirmed by electron microscopy. Antimycin-A (AMA)-induced injured proximal TEC (PK1 cells) were co-cultured with STC-like cells, STC-like cells-derived EV, or EV-free conditioned-medium for 3 days. Cellular injury, oxidative stress and mitochondrial function were assessed. Transfer of mitochondria from STC-like cells to TEC was assessed using Mito-trackers, and their viability by mitochondrial membrane potential assays. STC-like cells-derived EV were intra-arterially injected into mice 2 weeks after induction of unilateral renal artery stenosis. Two weeks later, renal hemodynamics were studied using magnetic-resonance-imaging, and renal fibrosis assessed ex-vivo . Cultured STC-like cells released EV that were uptaken by TEC. A protective effect conferred by STC-like cells in AMA-induced TEC injury was partly mimicked by their EV. Furthermore, STC-like cells-EV carried and transferred mitochondrial material to injured TEC, which partly restored mitochondrial function. In vivo , STC-like cells-derived EV engrafted in the stenotic kidney, and improved its perfusion and oxygenation. STC-like cells-EV exert protective effects on injured tubular cells in vitro and in vivo , partly by transferring STC-like cells mitochondria, which remain at least partly functional in recipient TEC.

Basal cell carcinoma (BCC), the most common skin cancer, is primarily driven by Hedgehog (Hh) and TP53 pathway alterations. Although additional pathways were implicated, the mutational landscape in Asian populations, particularly Koreans, remains underexplored. We performed whole-exome sequencing of BCC tumor tissues from Korean patients and analyzed mutations in 11 established BCC driver genes (PTCH1, SMO, GLI1, TP53, CSMD1/2, NOTCH1/2, ITIH2, DPP10, and STEAP4). Mutational profiles were compared with Caucasian cohort profiles to identify ethnicity-specific variants. Ultraviolet (UV)-exposed and non-UV-exposed tumor sites were compared; genes unique to non-UV-exposed tumors were further analyzed with protein–protein interaction analysis. BCCs in Koreans exhibited distinct features, including fewer truncating and more intronic variants compared to Caucasians. Korean-specific mutations in SMO, PTCH1, TP53, and NOTCH2 overlapped with oncogenic gain-of-function/loss-of-function (GOF/LOF) variants annotated in OncoKB, with some occurring at hotspot sites. BCCs in non-exposed areas showed recurrent mutations in CSMD1, PTCH1, and NOTCH1, suggesting a UV-independent mechanism. Novel mutations in TAS1R2 and ADCY10 were exclusive to non-exposed BCCs, with protein–protein interaction analysis linking them to TP53 and NOTCH2. We found unique ethnic-specific and UV-independent mutational profiles of BCCs in Koreans. TAS1R2 and ADCY10 may contribute to tumorigenesis of BCC in non-exposed areas, supporting the need for population-specific precision oncology.

Solar lentigo is a common hyperpigmented skin condition caused by chronic ultraviolet exposure, primarily affecting photoaged skin. While previous investigations focused on inflammatory and melanogenic mechanisms, the comprehensive role of lipid metabolism in pathogenesis remains unclear. We aimed to investigate systemic alterations in lipid metabolism and their contribution to solar lentigo development. We performed comprehensive analysis of RNA sequencing data from solar lentigo lesions and control skin samples (n = 7 per group) using metabolic flux simulations, gene co-expression networks, and protein-protein interaction analysis. These multi-system approaches were integrated to identify coordinated alterations in lipid metabolic pathways. Solar lentigo samples exhibited coordinated inhibition of fatty acid elongation, acetyl-CoA carboxylase activity, and sphingolipid biosynthesis, alongside impaired cholesterol synthesis via reduced squalene epoxidase and 7-dehydrocholesterol reductase activity. Compensatory upregulation of phospholipid synthesis enzymes and dihydroceramide desaturases was observed. Pathway disruption and altered calcium signaling, indicating aberrant cellular energy metabolism and membrane integrity. These findings suggest that solar lentigo pathogenesis involves systematic lipid metabolism dysregulation beyond melanogenesis, potentially contributing to membrane instability, energy homeostasis disruption and redox imbalance. The identification of specific metabolic bottlenecks reveals novel targets for lipid-based therapeutic approaches in pigmentary diseases.

The time at which hypertension treatment should be initiated for different age groups and sexes remains controversial. We aimed to determine whether the association between blood pressure (BP) and major adverse cardiovascular events (MACE) varies with age and sex. This study enrolled 327,328 subjects who had not taken antihypertensive medication in the Korean National Health Service-National Health Screening Cohort between 2002 and 2003. Participants were categorized into four groups according to 2017 American College of Cardiology/American Heart Association hypertension guideline. Primary outcome was MACE characterized by cardiovascular mortality, myocardial infarction, unstable angina, and stroke. During a 10-year follow-up, a significant increase in MACE risk was observed from the stage 1 hypertension group (hazard ratio [HR], 1.23; 95% CI 1.15–1.32; P  < 0.001) in time-varying Cox analysis. This relationship was persistent in subjects aged < 70 years, but increased MACE risk was observed only in the stage 2 hypertension group in ≥ 70 years (HR, 1.52; 95% CI 1.32–1.76, P  < 0.001). When categorized as per sex, both men and women showed significant MACE risk from stage 1 hypertension. However, on comparing the sexes after stratifying by age, a significantly increased risk of MACE was shown from stage 1 hypertension in men aged < 50 years, but from stage 2 hypertension in men aged ≥ 50 years. Meanwhile, increased MACE risk was observed from stage 2 hypertension in women aged < 60 years, but from stage 1 hypertension in women aged ≥ 60 years. Thus, young male subjects had higher MACE risk than young female subjects, but this difference gradually decreased with age and there was no difference between sexes in subjects aged ≥ 70 years. Therefore, our results suggest that hypertension treatment initiation may need to be individualized depending on age and sex.

Background Extracellular matrix (ECM) components promote the development of skin wounds by providing biological scaffolds and regenerative microenvironments. Aims To evaluate the beneficial effects of human dermal fibroblast‐derived ECM after fractional carbon dioxide laser resurfacing in Asians. Patients/Methods In this double‐blind, randomized, vehicle‐controlled, split‐face study, 15 participants with features of facial skin aging were treated with a single session of fractional carbon dioxide laser, followed by the application of either ECM (ECM group) or placebo (control group). In vivo skin parameters were measured at baseline and after 4 and 12 weeks of treatment using the Antera 3D®, Cutometer® MPA580, Dermascan®, and Tewameter®. Results A total of 14 participants (mean age 45.1 ± 9.7 years) completed the study. The change in melanin level was significantly lower in the ECM group than in the control group at week 12 (p < 0.05). Transient increase in erythema level was observed at week 4 in the control group, and the change in the erythema level was greater in the control group than in the ECM group (p = 0.014). Though the ECM group showed improvements in the dermal density, texture, transepidermal water loss, marionette lines (volume, maximum depth, and average depth), and nasolabial folds (volume, maximum depth, and length), no significant differences were found between the two groups. Treatment‐related adverse events were not reported. Conclusions We suggest that human dermal fibroblast‐derived ECM may be used as adjunctive therapy after fractional carbon dioxide resurfacing to prevent postinflammatory hyperpigmentation in Asians.

It is expected that artificial intelligence (AI) will be used extensively in the medical field in the future. The purpose of this study is to investigate the awareness of AI among Korean doctors and to assess physicians' attitudes toward the medical application of AI. We conducted an online survey composed of 11 closed-ended questions using Google Forms. The survey consisted of questions regarding the recognition of and attitudes toward AI, the development direction of AI in medicine, and the possible risks of using AI in the medical field. A total of 669 participants completed the survey. Only 40 (5.9%) answered that they had good familiarity with AI. However, most participants considered AI useful in the medical field (558/669, 83.4% agreement). The advantage of using AI was seen as the ability to analyze vast amounts of high-quality, clinically relevant data in real time. Respondents agreed that the area of medicine in which AI would be most useful is disease diagnosis (558/669, 83.4% agreement). One possible problem cited by the participants was that AI would not be able to assist in unexpected situations owing to inadequate information (196/669, 29.3%). Less than half of the participants(294/669, 43.9%) agreed that AI is diagnostically superior to human doctors. Only 237 (35.4%) answered that they agreed that AI could replace them in their jobs. This study suggests that Korean doctors and medical students have favorable attitudes toward AI in the medical field. The majority of physicians surveyed believed that AI will not replace their roles in the future.

Antioxidants may modulate the microenvironment of epidermal stem cells by reducing the production of reactive oxygen species or by regulating the expression of extracellular matrix protein. The extracellular membrane is an important component of the stem cell niche, and microRNAs regulate extracellular membrane-mediated basal keratinocyte proliferation. In this narrative review, we will discuss several antioxidants such as ascorbic acid, plant extracts, peptides and hyaluronic acid, and their effect on the epidermal stem cell niche and the proliferative potential of interfollicular epidermal stem cells in 3D skin equivalent models.

Abnormal histone modification by histone deacetylases (HDACs), including HDAC1 and sirtuin 1 (SIRT1), has been reported to play an important role in the pathogenesis of psoriasis by altering cell proliferation, differentiation, and inflammation. However, findings on the expression level of HDACs in psoriatic skin lack consistency. We assessed the expression of HDAC1, SIRT1, p63, and proliferating cell nuclear antigen (PCNA) in skin tissues from 23 patients with psoriasis (15 with plaque psoriasis and eight with guttate psoriasis) and five healthy individuals using immunohistochemistry, and analyzed their associations with clinical phenotypes of the disease. The expression of HDAC1 and keratinocyte proliferative markers, such as p63 and PCNA significantly increased, whereas that of SIRT1 decreased in the basal layer (p < 0.05) of the patients with psoriasis compared to those in healthy controls. Among the patients with psoriasis, expression of HDAC1, p63, and PCNA was significantly higher in plaque psoriasis than in guttate psoriasis. There was no significant differences in the level of SIRT1 between the two clinical phenotypes. The findings of this study suggest that histone modifications are involved in the pathogenesis of psoriasis and may contribute to the formation of clinical phenotypes.