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Molecular Research Progress of Skin and Skin Diseases: 2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 September 2025 | Viewed by 4020

Special Issue Editor


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Guest Editor
Department of Dermatology, Seoul St. Mary’s Hospital, College of Medicine College of Medicine, The Catholic University of Korea, 222, Banpo-daero, Seocho-gu, Seoul 06591, Republic of Korea
Interests: atopic dermatitis; psoriasis; inflammatory; skin disease
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Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of our previous Special Issue, “Molecular Research Progress of Skin and Skin Diseases”, published in 2023–2024.

Skin diseases, including skin cancer and inflammatory skin conditions such as atopic dermatitis, psoriasis, hair loss, and acne, are among the most chronic and difficult-to-treat conditions which constantly challenge dermatologists. Refractory patients always have an unmet need for innovative and effective new treatments. With advances in evidence-based molecular research, these therapies are being developed and are actively being investigated in clinical trials. Therefore, this Special Issue, titled “Molecular Research Progress of Skin and Skin Diseases”, aims to highlight the molecular biological advances that are currently being made in the treatment of skin and skin diseases and their use in patient care. In this issue, we welcome papers that focus on emerging pathogenic mechanisms in skin disease research, reviewing them, and exploring the promise of therapeutics targeting them. We hope to provide new inspiration for better understanding skin and skin diseases and for better treating them.

Dr. Ji Hyun Lee
Guest Editor

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Keywords

  • atopic dermatitis
  • psoriasis
  • alopecia
  • vitiligo
  • acne
  • skin cancer
  • JAK-STAT
  • inflammatory skin disease

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Published Papers (4 papers)

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Research

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18 pages, 3083 KiB  
Article
Targeting Vascular and Inflammatory Crosstalk: Cannabigerol as a Dual-Pathway Modulator in Rosacea
by Suji Kim and Ji Hyun Lee
Int. J. Mol. Sci. 2025, 26(14), 6840; https://doi.org/10.3390/ijms26146840 - 16 Jul 2025
Viewed by 378
Abstract
Rosacea is a chronic inflammatory skin condition characterized by persistent erythema and abnormal vascular response. Although current treatments focus on symptomatic relief, they often provide only temporary improvement and may be associated with side effects or recurrence. Cannabigerol (CBG), a non-psychoactive cannabinoid, has [...] Read more.
Rosacea is a chronic inflammatory skin condition characterized by persistent erythema and abnormal vascular response. Although current treatments focus on symptomatic relief, they often provide only temporary improvement and may be associated with side effects or recurrence. Cannabigerol (CBG), a non-psychoactive cannabinoid, has recently garnered attention for its pharmacological activities, including anti-inflammatory, antioxidant, neuroprotective, and skin barrier–supportive effects. However, its role in modulating pathological responses in rosacea remains unclear. In this study, we investigated the therapeutic potential of topically applied CBG in an LL-37-induced rosacea-like mouse model. Clinical and histological assessments revealed that CBG markedly reduced erythema, epidermal hyperplasia, and mast cell infiltration. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) showed downregulation of Il1b, Il4, Il6, Il13, Il22, Il31, Tlr2, Vegfa, and Mmp9. Immunohistochemistry and Western blot analyses further demonstrated suppression of CD31, vascular endothelial growth factor (VEGF), and Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ), along with reduced activation of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway, including decreased levels of JAK1, STAT3, and phosphorylated STAT3. These findings suggest that topical CBG alleviates rosacea-like skin inflammation by targeting inflammatory and vascular pathways, including JAK/STAT and YAP/TAZ signaling. Full article
(This article belongs to the Special Issue Molecular Research Progress of Skin and Skin Diseases: 2nd Edition)
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7 pages, 606 KiB  
Communication
Identification of Two Distinct Stem Cell Clusters, Lrig1-Derived and Wnt/CD44-Dependent, in Corneal Epithelium
by Laurent Barnes, Evangelia Konstantinou, Jean-Hilaire Saurat, Alexandre Moulin and Gürkan Kaya
Int. J. Mol. Sci. 2025, 26(13), 6383; https://doi.org/10.3390/ijms26136383 - 2 Jul 2025
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Abstract
We previously showed that selective suppression of CD44 in the corneal epithelium leads to structural abnormalities in the mouse cornea. Our comparative studies of young and aged ocular biopsies revealed that CD44 expression is downregulated in aged corneas, while leucine-rich repeats and immunoglobulin-like [...] Read more.
We previously showed that selective suppression of CD44 in the corneal epithelium leads to structural abnormalities in the mouse cornea. Our comparative studies of young and aged ocular biopsies revealed that CD44 expression is downregulated in aged corneas, while leucine-rich repeats and immunoglobulin-like domain 1 (Lrig1+) stem cells remain preserved in the peripheral limbus. These findings suggest an age-related shift in the corneal stem cell compartmentalization, characterized by impaired CD44 expression in the central cornea and preservation of Lrig1+ stem cells in the limbus, which become the main stem cells in the senescent cornea. To investigate this further, we performed topical tamoxifen-inducible, diphtheria toxin-mediated ablation of Lrig1+ stem cells in mouse corneas. We then assessed both activated and non-activated beta-catenin expression in wild-type (WT) and CD44 knockout (CD44KO) mice, given that CD44 modulates the Wingless-related integration site (Wnt) pathway. Our results indicate that two distinct stem cell populations operate in the mouse cornea: Lrig1-derived stem cells and Wnt-activity/CD44-dependent stem cells. The Lrig1-derived cells act as a reservoir of quiescent stem cells that regenerate the cornea upon injury, whereas under homeostatic conditions, the Wnt-activity/CD44-dependent stem cells are primarily responsible for corneal renewal. In the aged cornea, the loss of CD44 expression leads to reduced Wnt signaling, making the tissue increasingly dependent on Lrig1+ stem cells for regeneration. In mice, Lrig1+ stem cells are capable of sustaining permanent corneal renewal, even in the absence of CD44. Full article
(This article belongs to the Special Issue Molecular Research Progress of Skin and Skin Diseases: 2nd Edition)
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19 pages, 3061 KiB  
Article
Association of Genetic Polymorphisms in SLC45A2, TYR, HERC2, and SLC24A in African Women with Melasma: A Pilot Study
by Nomakhosi Mpofana, Zinhle Pretty Mlambo, Mokgadi Ursula Makgobole, Ncoza Cordelia Dlova and Thajasvarie Naicker
Int. J. Mol. Sci. 2025, 26(3), 1158; https://doi.org/10.3390/ijms26031158 - 29 Jan 2025
Viewed by 2348
Abstract
Melasma is a chronic skin disorder characterized by hyperpigmentation, predominantly affecting women with darker skin types, including those of African descent. This study investigates the association between genetic variants in SLC45A2, TYR, HERC2, and SLC24A5 genes and the severity of [...] Read more.
Melasma is a chronic skin disorder characterized by hyperpigmentation, predominantly affecting women with darker skin types, including those of African descent. This study investigates the association between genetic variants in SLC45A2, TYR, HERC2, and SLC24A5 genes and the severity of melasma in women of reproductive age. Forty participants were divided into two groups: twenty with facial melasma and twenty without. Deoxyribonucleic acid (DNA) was extracted from blood samples and genotyped using TaqMan assays to identify allele frequencies and genotype distributions. Significant associations were observed for the TYR gene (rs1042602), HERC2 gene (rs1129038), and SLC24A5 gene (rs1426654) polymorphisms, highlighting their potential roles in melasma susceptibility. For example, the rs1042602 Single Nucleotide Polymorphisms (SNP) in the TYR gene showed a strong association with melasma, with the AA genotype conferring a markedly increased risk. Similarly, the rs1129038 SNP in the HERC2 gene and the rs1426654 SNP in the SLC24A5 gene revealed significant genetic variations between groups in women of African descent. These findings underscore the influence of genetic polymorphisms on melasma’s pathogenesis, emphasizing the need for personalized approaches to its treatment, particularly for women with darker skin types. Full article
(This article belongs to the Special Issue Molecular Research Progress of Skin and Skin Diseases: 2nd Edition)
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Review

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21 pages, 7617 KiB  
Review
Transcriptomic Signatures and Molecular Pathways in Hidradenitis Suppurativa—A Narrative Review
by Jasmine Spiteri, Dillon Mintoff, Laura Grech and Nikolai P. Pace
Int. J. Mol. Sci. 2025, 26(16), 7704; https://doi.org/10.3390/ijms26167704 - 9 Aug 2025
Viewed by 303
Abstract
Hidradenitis suppurativa (HS) is a chronic, relapsing inflammatory dermatosis of the pilosebaceous unit characterized by nodules, abscesses, and dermal tunnels. Recent transcriptomic studies have implicated dysregulation of innate and adaptive immune responses, epidermal barrier dysfunction, and systemic metabolic alterations. This review synthesizes findings [...] Read more.
Hidradenitis suppurativa (HS) is a chronic, relapsing inflammatory dermatosis of the pilosebaceous unit characterized by nodules, abscesses, and dermal tunnels. Recent transcriptomic studies have implicated dysregulation of innate and adaptive immune responses, epidermal barrier dysfunction, and systemic metabolic alterations. This review synthesizes findings from 16 studies investigating the HS transcriptome using bulk and single-cell RNA sequencing. Differential gene expression analyses revealed extensive upregulation of inflammatory cytokines and chemokines, particularly in lesional and perilesional skin. These changes were also mirrored in non-lesional skin, suggesting diffuse immune dysregulation beyond visibly affected areas. Downregulated pathways include those involved in lipid metabolism, muscle contraction, and neuronal signaling, potentially linking HS to obesity, metabolic syndrome, and neuropsychiatric comorbidities. Single-cell transcriptomics confirmed the enrichment of keratinocytes and immune cells (B cells, plasma cells, M1 macrophages, and T cells) with proinflammatory profiles in HS lesions. Keratinocyte dysfunction further implicated a compromised epidermal barrier in disease pathogenesis. While transcriptomic studies have advanced mechanistic understanding and highlighted therapeutic targets—such as the IL-1β–TH17 axis and B cell signaling pathways—methodological heterogeneity limits cross-study comparisons. Integration of multi-omics data and standardized phenotyping will be essential to identify robust biomarkers, stratify HS subtypes, and guide personalized therapeutic approaches. Full article
(This article belongs to the Special Issue Molecular Research Progress of Skin and Skin Diseases: 2nd Edition)
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