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Exploring Molecular Pathways in Skin Health and Diseases
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Exploring Molecular Pathways in Skin Health and Diseases

A Special Issue of Current Issues in Molecular Biology (ISSN 1467-3045) belonging to the section "Biochemistry, Molecular and Cellular Biology".

Deadline for manuscript submissions: closed (20 August 2026) | Viewed by 13924

Editor

Dr. Sullim Lee

E-Mail Website
Guest Editor
Department of Life Science, College of Bio-Nano Technology, Gachon University, Seongnam, Republic of Korea
Interests: oxidative stress; inflammation; antioxidant effect; anti-inflammatory effect; anti-skin aging; skin disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Skin health is regulated by complex molecular pathways that preserve its structure and function while enabling responses to internal and external stressors. These pathways play pivotal roles in processes such as oxidative stress regulation, cytokine signaling, collagen metabolism, and immune responses, which are crucial in maintaining skin homeostasis. However, disruptions to these pathways can result in various skin conditions, including chronic inflammation, premature aging, and skin cancer.

This Special Issue will explore the molecular mechanisms underpinning skin health and disease, focusing on cutting-edge research in this field. A particular emphasis will be placed on the discovery of biomarkers and the development of innovative therapeutic strategies to elucidate the causes of skin diseases and identify potential treatments.

By addressing these critical topics, this Special Issue will provide novel insights into skin biology and facilitate the advancement of effective prevention and treatment approaches. We invite submissions spanning a wide range of research areas, from basic science to clinical applications, with the aim of fostering significant contributions to the study of skin health and disease.

Dr. Sullim Lee
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Current Issues in Molecular Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2400 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • skin health
  • skin aging
  • skin disease
  • molecular pathways
  • oxidative stress
  • immune response
  • inflammatory skin diseases

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Published Papers (7 papers)

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Research

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16 pages, 13006 KB  
Article
Regulation of Imiquimod-Induced Mouse Psoriasis Development via Apoptosis Signal-Regulating Kinase 1 Potentially by Antagonizing Aryl Hydrocarbon Receptor Expression
by Hideaki Hasegawa, Aruma Watanabe, Yasuhiro Katahira, Izuru Mizoguchi, Tatsuo Maeda, Junya Mizugami, Isao Naguro, Hidenori Ichijo, Kazutoshi Harada, Yukari Okubo and Takayuki Yoshimoto
Curr. Issues Mol. Biol. 2026, 48(7), 653; https://doi.org/10.3390/cimb48070653 - 25 Jun 2026
Viewed by 516
Abstract
Imiquimod-induced skin inflammation is the most widely used psoriasis mouse model. Although p38 mitogen-activated protein kinase reportedly plays a role in the pathogenesis of psoriatic inflammation, the purpose of one of its upstream activators, apoptosis signal-regulating kinase 1 (ASK1), remains unclear. This study [...] Read more.
Imiquimod-induced skin inflammation is the most widely used psoriasis mouse model. Although p38 mitogen-activated protein kinase reportedly plays a role in the pathogenesis of psoriatic inflammation, the purpose of one of its upstream activators, apoptosis signal-regulating kinase 1 (ASK1), remains unclear. This study investigated the role of ASK1 and its molecular mechanism in the imiquimod-induced psoriasis model. Compared to wild-type mice, the ASK1 knockout (KO) mouse skin lesion showed a higher clinical score and a thicker epidermis. The mRNA expression of pro-inflammatory cytokines, such as IL-17 and TNF-α, was also higher. Notably, the expression of aryl hydrocarbon receptor (AhR), a sensor for xenobiotic chemicals that is expressed in the skin to strengthen the skin barrier and accelerate terminal differentiation of the epidermis—as well as its downstream molecule CYP1A1, but not NRF2—was increased in the ASK1 KO psoriatic skin lesion. Immunoprecipitation analysis, followed by Western blotting, revealed that ASK1 interacts with AhR in cells transfected with their respective expression vectors, potentially leading to reduced AhR expression. These results suggest that ASK1 negatively regulates the development of the imiquimod-induced mouse psoriasis model by interacting with AhR and presumably antagonizing the AhR-CYP1A1 axis. Full article
(This article belongs to the Special Issue Exploring Molecular Pathways in Skin Health and Diseases)
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13 pages, 1228 KB  
Article
Multi-Target Restoration of Dermal Elastic Fibers Through Elastin Upregulation, Elastase Suppression, and Scaffold Reinforcement
by Sanghyun Ye, Seongsu Kang, Eui Taek Jeong, Seung-Hyun Jun and Nae-Gyu Kang
Curr. Issues Mol. Biol. 2026, 48(5), 431; https://doi.org/10.3390/cimb48050431 - 22 Apr 2026
Viewed by 1459
Abstract
Elastic fibers are key components of the skin extracellular matrix and are essential for maintaining skin integrity and elasticity. During skin aging, particularly photoaging, elastic fiber integrity is progressively compromised by increased elastase activity and the downregulation of elastin and scaffold-related gene expression. [...] Read more.
Elastic fibers are key components of the skin extracellular matrix and are essential for maintaining skin integrity and elasticity. During skin aging, particularly photoaging, elastic fiber integrity is progressively compromised by increased elastase activity and the downregulation of elastin and scaffold-related gene expression. Therefore, effective strategies to preserve elastic fiber function should address not only elastin synthesis but also enzymatic degradation and scaffold integrity. In this study, we investigated a multitarget approach to restoring the elastic fiber network by modulating elastin production, elastase activity, and scaffold protein expression. We found that Copper Tripeptide-1 enhanced elastin expression and secretion, ethyl ferulate inhibited elastase activity, and cedrol promoted scaffold-related gene expression and microfibrillar protein restoration in dermal fibroblasts. To assess the biological relevance of this approach, the combined treatment was evaluated using UV-damaged human skin biopsy samples. This combination effectively mitigated UV-induced elastic fiber disruption and significantly improved fiber architecture, as confirmed by immunofluorescence staining and scanning electron microscopy. These findings indicate that coordinated modulation of elastin production, proteolytic protection, and scaffold reinforcement is essential for maintaining elastic fiber integrity and represents a promising approach for preserving skin elasticity during aging. Full article
(This article belongs to the Special Issue Exploring Molecular Pathways in Skin Health and Diseases)
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15 pages, 2763 KB  
Article
Modulation of Corticotropin-Releasing Hormone Receptor Expression During In Vitro Keratinocyte Differentiation
by Carole-Anne Martins, Sara Lesink, Angéline Roux, Guillaume Collet and Richard Daniellou
Curr. Issues Mol. Biol. 2026, 48(2), 210; https://doi.org/10.3390/cimb48020210 - 14 Feb 2026
Cited by 1 | Viewed by 976
Abstract
Corticotropin-releasing hormone (CRH) and its receptors CRHR1 and CRHR2 are major actors in the stress response and are well established as components of the hypothalamic–pituitary–adrenal (HPA) axis. Evidence also suggests they are expressed in peripheral tissues and, more interestingly, in the skin. While [...] Read more.
Corticotropin-releasing hormone (CRH) and its receptors CRHR1 and CRHR2 are major actors in the stress response and are well established as components of the hypothalamic–pituitary–adrenal (HPA) axis. Evidence also suggests they are expressed in peripheral tissues and, more interestingly, in the skin. While CRHR1 expression in keratinocytes is documented in terms of presence or absence, data on CRHR2 remain sparse. Moreover, there is no detailed description of the exact localization of CRHR1/2 receptors within the different layers of the epidermis, leaving this question fully unexplored. To better understand the link between stress and skin disorders, we aimed to investigate the differential expression of CRHR1 and CRHR2 in keratinocytes, depending on their level of differentiation. In vitro results demonstrated that CRHR1 appears to be more abundant at early stages of differentiation and CRHR2 at more advanced stages. Full article
(This article belongs to the Special Issue Exploring Molecular Pathways in Skin Health and Diseases)
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14 pages, 1378 KB  
Article
A Liposomal Formulation Enhances the Anti-Senescence Properties of Nicotinamide Adenine-Dinucleotide (NAD+) in Endothelial Cells and Keratinocytes
by Stefano Ministrini, Luca Liberale, Hanns-Eberhard Erle, Giuseppe Percoco, Ali Tfayli, Ali Assi, Ivan Kapitonov, Isabel Greiner and Giovanni Guido Camici
Curr. Issues Mol. Biol. 2025, 47(9), 722; https://doi.org/10.3390/cimb47090722 - 5 Sep 2025
Cited by 3 | Viewed by 7146
Abstract
Nicotinamide adenine-dinucleotide (NAD+) supplementation is a promising strategy to delay cellular aging in different areas, including cosmetic dermatology. However, low bioavailability and stability of NAD+ formulations are the main factors limiting its effectiveness as an anti-aging treatment. In light of [...] Read more.
Nicotinamide adenine-dinucleotide (NAD+) supplementation is a promising strategy to delay cellular aging in different areas, including cosmetic dermatology. However, low bioavailability and stability of NAD+ formulations are the main factors limiting its effectiveness as an anti-aging treatment. In light of the above, a liposomal formulation of NAD+ (LF-NAD+) was tested in this study and compared to NAD+ alone in primary human aortic endothelial cells (HAECs) and primary human epidermal keratinocytes (HEKas). Intracellular NAD+ was measured using a colorimetric assay. Cell survival was derived from lactate dehydrogenase release in supernatants. Cell senescence was measured by senescence-associated β-galactosidase staining. Molecular mechanisms underlying the reported effects were analyzed by Western blot. Skin penetration of NAD+ was measured ex vivo in skin explants, using infrared spectroscopy. Compared to control NAD+ alone, the LF-NAD+ formulation increased the intracellular NAD+ content and cell survival in HAECs, but not in HEKas. Instead, a significant reduction in the number of senescent cells was observed in both HAECs and HEKas. LF-NAD+ treatment was associated with a reduced expression of p16 in both HAECs and HEKas, and to a significant reduction in p21 in HEKas alone. Finally, LF-NAD+ increases the skin penetration of the active substance NAD+ by 30% compared to the application of NAD+ alone. LF-NAD+, enhances the anti-aging effects of NAD+ on vascular and skin cells. Such in vitro findings might indicate a potential anti-aging role in the microcirculation and in the epidermidis. Full article
(This article belongs to the Special Issue Exploring Molecular Pathways in Skin Health and Diseases)
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18 pages, 2683 KB  
Article
Evaluation of the Antiaging Potential of the Dendropanax morbiferus-Derived Compound Dendropanoxide in TNF-α-Stimulated Human Dermal Fibroblasts
by Si-Young Ahn, Sanghyun Lee, Daeyoung Kim and Sullim Lee
Curr. Issues Mol. Biol. 2025, 47(3), 188; https://doi.org/10.3390/cimb47030188 - 14 Mar 2025
Cited by 2 | Viewed by 1914
Abstract
In this study, we investigated the antiaging potential of dendropanoxide (DP), an active compound derived from Dendropanax morbiferus, in human dermal fibroblasts (NHDFs) induced by Tumor Necrosis Factor-alpha (TNF-α) and in human epidermal keratinocytes (NHEKs) induced by TNF-α and interferon gamma (IFN-γ). [...] Read more.
In this study, we investigated the antiaging potential of dendropanoxide (DP), an active compound derived from Dendropanax morbiferus, in human dermal fibroblasts (NHDFs) induced by Tumor Necrosis Factor-alpha (TNF-α) and in human epidermal keratinocytes (NHEKs) induced by TNF-α and interferon gamma (IFN-γ). We induced oxidative stress related to ultraviolet (UV) radiation with TNF-α and IFN-γ and then treated the cells with various concentrations of DP to evaluate its effects on reactive oxygen species (ROS) production, matrix metalloproteinase-1 (MMP-1) expression, collagen synthesis, inflammatory cytokine expression, and skin barrier protection. The results showed that DP significantly reduced ROS production, indicating its potential to alleviate oxidative stress in the skin. Additionally, DP effectively inhibited MMP-1 production, suggesting that it could prevent collagen degradation in the dermis, significantly increase the secretion of pro-collagen I, promote collagen synthesis, and protect the dermal extracellular matrix (ECM). Moreover, DP significantly reduced the expression of inflammatory cytokines IL-1β and IL-6, thereby inhibiting excessive inflammatory responses in the skin. DP also enhanced the gene expression of key factors involved in skin barrier maintenance, including Kazal-type 5 (SPINK5), loricrin (LOR), aquaporin-3 (AQP3), filaggrin (FLG), and keratin 1 (KRT1), suggesting its potential to maintain and protect the skin barrier. Western blot analysis revealed that DP inhibited TNF-α-induced phosphorylation of JNK and p38, implying that DP exerts antiaging effects through the regulation of the JNK and p38 signaling pathways. Collectively, these findings suggest that DP has significant potential as an antiaging agent. Full article
(This article belongs to the Special Issue Exploring Molecular Pathways in Skin Health and Diseases)
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Review

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23 pages, 710 KB  
Review
The Influence of Sunscreen Use on Skin Pigmentation Disorders: Melasma, Post-Inflammatory Hyperpigmentation, and Vitiligo
by Bruna Azevedo, Margarida Lorigo and Elisa Cairrao
Curr. Issues Mol. Biol. 2026, 48(9), 921; https://doi.org/10.3390/cimb48090921 - 9 Sep 2026
Viewed by 314
Abstract
Skin pigmentation is influenced by multiple factors, with sun exposure being one of the most important. Therefore, sun protection plays a central role in the prevention and treatment of pigmentation disorders. This work analysed the recent literature (2015–2025) on the influence of sun [...] Read more.
Skin pigmentation is influenced by multiple factors, with sun exposure being one of the most important. Therefore, sun protection plays a central role in the prevention and treatment of pigmentation disorders. This work analysed the recent literature (2015–2025) on the influence of sun protection in melasma, post-inflammatory hyperpigmentation, and vitiligo, highlighting therapeutic advances and the impact of sunscreen use in both the prevention and treatment of these conditions. A search was conducted in the PubMed and SCOPUS databases using MeSH terms, selecting original research studies in English and employing various methodologies. Conventional sun protection (UVB/UVA) may not be sufficient on its own to prevent skin pigmentation disorders, given the evidence supporting a role for UVA1 radiation and blue light (380–455 nm) in inducing hyperpigmentation, especially in individuals with phototypes IV-VI. Innovative, broad-spectrum sunscreens, e.g., iron oxide and methoxypropylaminocyclohexenylidene ethoxyethylcyanoacetate, have shown potential for enhancing protection against hyperpigmentation in visible light, while some tinted formulations may also provide cosmetic benefits by camouflaging existing dark spots. The discrepancy between the application doses used compromises observed efficacy, reinforcing the need for public education on photoprotection and for research conducted under real-use conditions. Personalised strategies that combine broad-spectrum and visible-light protection with antioxidant and anti-inflammatory agents may optimise the prevention and management of these disorders. Full article
(This article belongs to the Special Issue Exploring Molecular Pathways in Skin Health and Diseases)
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23 pages, 1618 KB  
Review
Microbial Dysbiosis in Photodermatoses: Formation, Pathogenesis and Intervention Strategies
by Lanhai Zhong, Tian Wang, Lu Tang, Jiande Han, Qun Zhao and Naiyu Lin
Curr. Issues Mol. Biol. 2026, 48(5), 493; https://doi.org/10.3390/cimb48050493 - 9 May 2026
Cited by 1 | Viewed by 638
Abstract
Recent studies have reported skin microbiome dysbiosis in patients with photodermatoses, featuring enriched Staphylococcus aureus colonization and decreased microbiome diversity. We propose that ultraviolet radiation (UVR), along with atypical antimicrobial peptides, may exert selective pressure on the skin microbiome, while cytokine dysregulation and [...] Read more.
Recent studies have reported skin microbiome dysbiosis in patients with photodermatoses, featuring enriched Staphylococcus aureus colonization and decreased microbiome diversity. We propose that ultraviolet radiation (UVR), along with atypical antimicrobial peptides, may exert selective pressure on the skin microbiome, while cytokine dysregulation and a reduction in commensal bacteria amplify microbial dysbiosis. Dysbiotic microorganisms further release pathogen-associated patterns and virulence factors, and activate tissue-resident memory T cells, which collectively contribute to local inflammation. These mechanisms establish the skin microbiome as a potential target for early intervention. Potential therapeutic strategies may include antibiotics, phototherapy, bleach baths, phage therapy, and microbiota-based therapies. This review integrates current findings from microbial ecology, molecular biology, and host immunology to outline a conceptual framework linking UVR exposure, microbiome alterations, and cutaneous immune responses, while emphasizing the current limitations and evidence gaps in this field. Full article
(This article belongs to the Special Issue Exploring Molecular Pathways in Skin Health and Diseases)
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