Journal of dermatological science最新文献

{"title":"COMMD3 mediates melanin synthesis through both clusterin-PAX3 axis and copper-dependent tyrosinase activity in skin pigmentation","authors":"Xinyi Huang,&nbsp;Shan Wu,&nbsp;Min Yan,&nbsp;Shengzhe Zhou,&nbsp;Jiadie Wang,&nbsp;Jianghan Li,&nbsp;Min Yao","doi":"10.1016/j.jdermsci.2026.04.005","DOIUrl":"10.1016/j.jdermsci.2026.04.005","url":null,"abstract":"<div><h3>Background</h3><div>Pigmentation-related disorders mainly revolve around abnormal melanogenesis, but the regulatory mechanisms remain unclear. Recent reports have found that COMMD3 plays a role in promoting melanin synthesis.</div></div><div><h3>Objectives</h3><div>This study aims to investigate the molecular mechanisms and relation with copper homeostasis of a novel pigment-promoting gene, <em>COMMD3</em>, in skin pigmentation.</div></div><div><h3>Methods</h3><div>A UV-induced pigmentation murine model was created by UVB irradiation for examining the function of COMMD3 in acquired hyperpigmentation. Intracellular copper content was measured to determine the effect of COMMD3 on tyrosinase activity. After suppressing COMMD3 by gene knockdown (KD) in the B16F10 cell line and the UVB-induced pigmented murine model, RNA sequencing was conducted to identify potential signaling pathways underlying COMMD3 regulating melanogenesis.</div></div><div><h3>Results</h3><div>COMMD3 modulating melanogenesis was observed in UV-induced pigmented murine models and B16F10s. RNA sequencing and validation supported that suppressing COMMD3 leads to an increase in clusterin (CLU), decreasing PAX3 and its nuclear translocation, ultimately resulting in a reduction of melanogenesis. Concurrently, as a copper transporter, a decrease in COMMD3 expression caused intracellular copper accumulation, which lowered tyrosinase activity and reduced melanin production. After using the copper chelator ammonium tetrathiomolybdate to alleviate copper accumulation caused by COMMD3 deficiency, repress CLU expression, and restore PAX3, leading to increasing melanin content in melanogenesis.</div></div><div><h3>Conclusion</h3><div>Our findings demonstrate that COMMD3 plays an important role in regulating melanogenesis. COMMD3 regulates melanogenesis via CLU-PAX3 axis and adjusts tyrosinase activity through intracellular copper levels. The insights provide a mechanistic rationale and potential therapeutic strategy for mitigating acquired skin pigmentation disorders.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"123 1","pages":"Pages 27-38"},"PeriodicalIF":4.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147978139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editors choice","authors":"","doi":"10.1016/S0923-1811(26)00113-1","DOIUrl":"10.1016/S0923-1811(26)00113-1","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"123 1","pages":"Page ii"},"PeriodicalIF":4.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148528991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Low Ki-67 marks immunogenic CD8⁺ tissue-resident memory T cell enrichment in vitiligo skin","authors":"Jing Wang,&nbsp;Kazunori Yokoi,&nbsp;Shoichi Matsuda,&nbsp;Hanako Koguchi-Yoshioka,&nbsp;Yosuke Ishitsuka,&nbsp;Rei Watanabe,&nbsp;Manabu Fujimoto,&nbsp;Atsushi Tanemura","doi":"10.1016/j.jdermsci.2026.05.004","DOIUrl":"10.1016/j.jdermsci.2026.05.004","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"123 1","pages":"Pages 43-47"},"PeriodicalIF":4.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147978179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective effects of the selective JAK2/3 inhibitor AG490 against ulcer formation following cutaneous ischemia-reperfusion injury","authors":"Shintaro Saito,&nbsp;Akihiko Uchiyama,&nbsp;Takeshi Araki,&nbsp;Yuta Inoue,&nbsp;Mayu Ohtaka,&nbsp;Keiji Kosaka,&nbsp;Takayuki Shuto,&nbsp;Azusa Ida,&nbsp;Yoko Yokoyama,&nbsp;Sachiko Ogino,&nbsp;Ryoko Torii,&nbsp;Yuki Watanuki,&nbsp;Akiko Sekiguchi,&nbsp;Sei-ichiro Motegi","doi":"10.1016/j.jdermsci.2026.03.004","DOIUrl":"10.1016/j.jdermsci.2026.03.004","url":null,"abstract":"<div><h3>Background</h3><div>Pressure ulcers are refractory skin ulcers that frequently develop at pressure sites in elderly individuals and those with reduced physical activity, and effective preventive strategies are urgently needed. These ulcers are primarily caused by cutaneous ischemia-reperfusion (I/R) injury, in which inflammation and oxidative stress play important roles. JAK inhibitors are widely used for inflammatory disorders and are also known to possess antioxidant effects. However, their therapeutic potential in cutaneous I/R injury remains unclear.</div></div><div><h3>Objective</h3><div>This study aimed to investigate the role of JAK/STAT signaling and the efficacy of the selective JAK2/3 inhibitor AG490 in preventing ulcer formation in a murine cutaneous I/R model.</div></div><div><h3>Methods</h3><div>In vivo, mice underwent four cycles of 3 h ischemia followed by 1 h reperfusion using magnetic skin compression. AG490 or vehicle was administered intraperitoneally before ischemia. In vitro, 10T1/2 cells were subjected to an oxygen–glucose deprivation/reoxygenation (OGD/R) model.</div></div><div><h3>Results</h3><div>Cutaneous I/R induced phosphorylation of JAK2 and STAT3, which was suppressed by AG490. On day 3, ulcer areas were significantly smaller in AG490-treated mice. AG490 also reduced inflammatory cell infiltration, apoptosis, and hypoxia, while enhancing Nrf2 activity in Keap1-dependent oxidative stress detector-luciferase (OKD-LUC) mice. In vitro, AG490 suppressed OGD/R-induced JAK/STAT activation, attenuated ROS production, prevented cell death, and enhanced the expression of HO-1.</div></div><div><h3>Conclusion</h3><div>We demonstrated the protective effect of AG490 against I/R-induced skin damage through the attenuation of inflammation and oxidative stress, highlighting JAK inhibition as a promising approach for pressure ulcer prevention.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"123 1","pages":"Pages 8-17"},"PeriodicalIF":4.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A SpliceAI-guided workflow for transcript validation using archived formalin-fixed paraffin-embedded skin tissue: Application to ATP2C1 splice-region variation in Hailey–Hailey disease","authors":"Haruna Goto,&nbsp;Yasuaki Ikuno,&nbsp;Miharu Shibata,&nbsp;Akihiko Yamaguchi,&nbsp;Toshifumi Takahashi,&nbsp;Akiko Arakawa,&nbsp;Yukie Kande,&nbsp;Hayato Naka-Kaneda,&nbsp;Noriki Fujimoto","doi":"10.1016/j.jdermsci.2026.05.003","DOIUrl":"10.1016/j.jdermsci.2026.05.003","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"123 1","pages":"Pages 39-42"},"PeriodicalIF":4.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147978147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unsaturated fatty acids mediate the bidirectional link between psoriasis and depression: Evidence from observational and mendelian randomization studies","authors":"Mengyang Chu,&nbsp;Biqing Tian,&nbsp;Jian Zhou,&nbsp;Guangquan Xu,&nbsp;Yunfeng Gu,&nbsp;Jiaqi Wang,&nbsp;Junfeng Hao,&nbsp;Erle Dang,&nbsp;Shuai Shao,&nbsp;Gang Wang","doi":"10.1016/j.jdermsci.2026.04.006","DOIUrl":"10.1016/j.jdermsci.2026.04.006","url":null,"abstract":"<div><h3>Background</h3><div>Depression is a prevalent and debilitating comorbidity of psoriasis. While the epidemiological association between the two conditions is well established, the causal relationship and the underlying biological mechanisms remain insufficiently understood.</div></div><div><h3>Objectives</h3><div>To evaluate the causal association between psoriasis and depression, as well as the mediating function of circulating unsaturated fatty acids (UFAs).</div></div><div><h3>Methods</h3><div>We combined cross-sectional analysis of 211 psoriasis patients, high-throughput serum metabolomics, and bidirectional Mendelian randomization (MR) using large-scale genome-wide association studies (9267 psoriasis cases; 170,756 depression cases). Multivariable MR analyses were adjusted for body mass index (BMI) and smoking. Two-step MR mediation was used to assess the role of UFA phenotypes.</div></div><div><h3>Results</h3><div>Clinically significant depressive symptoms (PHQ-9 ≥ 10) were present in 32.7% of patients and were independently associated with higher BMI, smoking, special site involvement, and higher PASI scores. MR analyses indicated a robust bidirectional causal relationship between psoriasis and depression, independent of BMI and smoking. Serum metabolomics revealed reduced omega-3 PUFAs (DHA, DPA, ETA) and elevated MUFAs in psoriasis patients with depression. Mediation MR identified the DHA-to-total fatty acid ratio as a key causal intermediary from psoriasis to depression, whereas depression liability altered PUFA/MUFA ratios to promote psoriasis risk.</div></div><div><h3>Conclusions</h3><div>Our integrative approach reveals a causal, bidirectional link between psoriasis and depression and indicates that unsaturated fatty acid imbalance, particularly reduced omega-3 PUFAs, may serve as a potential mediating mechanism. These findings highlight modifiable intervention targets, including weight management, smoking cessation, and omega-3 supplementation, may help to simultaneously improve dermatologic and psychiatric outcomes.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"123 1","pages":"Pages 1-7"},"PeriodicalIF":4.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147950577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heparinoid and phospho-pyridoxal preserve tight junction integrity in human skin under oxidative stress","authors":"Hiroki Sakamoto ,&nbsp;Ryota Asahina ,&nbsp;Momoyo Nishikawa ,&nbsp;Seigo Yamada ,&nbsp;Gyohei Egawa ,&nbsp;Kenji Kabashima","doi":"10.1016/j.jdermsci.2026.03.007","DOIUrl":"10.1016/j.jdermsci.2026.03.007","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"122 2","pages":"Pages 66-69"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147597209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editors choice","authors":"","doi":"10.1016/S0923-1811(26)00090-3","DOIUrl":"10.1016/S0923-1811(26)00090-3","url":null,"abstract":"","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"122 2","pages":"Page ii"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147827172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of eukaryotic translation initiation factor 1 A (eIF1A) and 3B (eIF3B) diminishes the psoriatic phenotype in two mouse models and human 3D model samples","authors":"Nicole Golob-Schwarzl ,&nbsp;Natalie Bordag ,&nbsp;Nitesh Shirsath ,&nbsp;Christin-Therese Müller ,&nbsp;Amin El-Heliebi ,&nbsp;Peter Wolf","doi":"10.1016/j.jdermsci.2026.03.008","DOIUrl":"10.1016/j.jdermsci.2026.03.008","url":null,"abstract":"<div><h3>Background</h3><div>Psoriasis is a systemic inflammatory skin disease for which new topical treatments are needed. Psoriatic inflammation is associated with overexpression of eukaryotic translation initiation factors (eIFs), which regulate gene expression in processes such as proliferation, apoptosis, and differentiation. However, their role in psoriasis remains unclear.</div></div><div><h3>Objective</h3><div>To investigate the contribution of eIF1A and eIF3B to psoriasis pathogenesis and evaluate the therapeutic potential of their inhibition via small interfering RNA (siRNA).</div></div><div><h3>Methods</h3><div>We used two mouse models reflecting different mechanisms of psoriasis: (i) topical application of imiquimod (IMQ) and (ii) K5.TGFβ transgenic mice promoting keratinocyte proliferation. eIF1A and eIF3B were inhibited by either topical or systemic siRNA administration. A 3D human psoriasis model was also used for validation.</div></div><div><h3>Results</h3><div>Inhibition of eIF1A and eIF3B reduced inflammation in both mouse models and the 3D human model. Downregulation of these factors normalized keratinocyte proliferation, epidermal thickness, and cytokine expression (e.g., TNFα, IL-1β, IL-17, IL-22). Differentiation markers such as KRT16 and FLG were restored. These findings suggest that eIF1A and eIF3B play a key role in maintaining the psoriatic inflammatory phenotype.</div></div><div><h3>Conclusion</h3><div>Our findings reveal a translational imbalance in psoriasis and identify eIF1A and eIF3B as crucial regulators of disease pathophysiology. Targeting these factors represents a promising new therapeutic strategy for psoriasis treatment.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"122 2","pages":"Pages 27-35"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147597279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell RNA sequencing identifies long non-coding RNAs enriched in psoriatic epidermal subsets","authors":"Longlong Luo ,&nbsp;Jan Cedric Freisenhausen ,&nbsp;Devin Malitha Dompage ,&nbsp;Huaitao Cheng ,&nbsp;Martin Enge ,&nbsp;Andor Pivarcsi ,&nbsp;Enikö Sonkoly","doi":"10.1016/j.jdermsci.2026.03.002","DOIUrl":"10.1016/j.jdermsci.2026.03.002","url":null,"abstract":"<div><h3>Background</h3><div>Psoriasis is a chronic inflammatory skin disease characterised by disrupted crosstalk between keratinocytes and immune cells, resulting in epidermal dysfunction. Long non-coding RNAs (lncRNAs) regulate gene expression in a cell- or tissue-specific manner, yet their role in psoriatic epidermal dysfunction remains poorly understood.</div></div><div><h3>Objectives</h3><div>To generate a single-cell atlas of lncRNA expression in healthy and psoriatic epidermis and identify cell state-specific lncRNAs associated with disease.</div></div><div><h3>Methods</h3><div>Data from Smart-seq2 single-cell RNA sequencing of sorted CD45⁺ and CD45⁻ epidermal cells from healthy controls and lesional/non-lesional psoriatic skin were analysed. Selected lncRNAs were validated by RT-qPCR, single-molecule <em>in situ</em> hybridisation (RNAscope), and immunofluorescence. The regulation of <em>LINC01137</em> was studied in IL-17A-treated primary keratinocytes and 3D epidermal models, and its function assessed using siRNA-mediated knockdown in keratinocytes.</div></div><div><h3>Results</h3><div>We identified 1412 epidermal lncRNAs with robust expression across distinct keratinocyte and immune cell states. LncRNAs exhibited strong cell type-specific expression in both keratinocytes and immune cells, moreover, several lncRNAs showed selective expression in psoriasis-associated cell states. <em>LINC01137</em> was enriched in activated keratinocytes, induced by IL-17A and correlated with TGF-β pathway activity; its knockdown in primary keratinocytes attenuated TGF-β-induced SERPINE1/PAI-1 expression. <em>LINC00892</em> was enriched in lesional Th1, Th17 and proliferating CD8⁺ T cells and showed increased expression as well as co-localisation with the T cell marker CD3 in psoriasis epidermis.</div></div><div><h3>Conclusions</h3><div>This study identifies the single-cell non-coding transcriptomic landscape of the psoriatic epidermis and highlights distinct lncRNA signatures in keratinocytes and immune cells, suggesting their involvement in pathogenic processes in psoriasis.</div></div>","PeriodicalId":94076,"journal":{"name":"Journal of dermatological science","volume":"122 2","pages":"Pages 36-46"},"PeriodicalIF":4.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147577358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}