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News in Skin Diseases: From Basic Mechanisms to Therapies
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News in Skin Diseases: From Basic Mechanisms to Therapies

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 May 2025 | Viewed by 6624

Special Issue Editor

Dr. Takemichi Fukasawa

E-Mail Website
Guest Editor
Department of Dermatology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan
Interests: systemic sclerosis; psoriasis; atopic dermatitis; myositis; SLE; vasculitis; B cells; T cells
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In recent years, advances have been made in the treatment of various inflammatory skin diseases that cause skin lesions, such as psoriasis, atopic dermatitis, and scleroderma. Many biologics targeting inflammatory cytokines and molecularly targeted drugs, such as JAK inhibitors, have emerged. The mechanisms of action and research on these drugs are advancing at a tremendous pace. These treatments are being studied from a variety of perspectives, including not only their therapeutic effect on skin lesions, but also their therapeutic effect on joints and their impact on other complications. In this Special Issue of IJMS, we will publish cutting-edge information regarding recent advances in the research of skin diseases from molecular viewpoints. We warmly welcome research and review articles concerning a variety of factors relating to skin diseases, including their genetic/epigenetic regulation, therapy, and prevention. In this Special Issue, we aim to present the latest findings regarding skin diseases, from basic mechanisms to therapies.

Dr. Takemichi Fukasawa
Guest Editor

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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 100 words) can be sent to the Editorial Office for announcement on this website.

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Keywords

  • skin diseases
  • psoriasis
  • atopic dermatitis
  • scleroderma
 

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Published Papers (4 papers)

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Research

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15 pages, 2020 KiB  
Article
Evaluation of Clobetasol and Tacrolimus Treatments in an Imiquimod-Induced Psoriasis Rat Model
by Philippe Guillaume, Tristan Rupp, Guillaume Froget and Sonia Goineau
Int. J. Mol. Sci. 2024, 25(17), 9254; https://doi.org/10.3390/ijms25179254 - 26 Aug 2024
Viewed by 946
Abstract
Psoriasis is a chronic inflammatory skin disorder characterized by keratinocyte hyperproliferation, inflammation, and aberrant differentiation. Imiquimod-induced psoriasis in rodent models has been widely used to study the pathogenesis of the disease and evaluate potential therapeutic interventions. In this study, we investigated the efficacy [...] Read more.
Psoriasis is a chronic inflammatory skin disorder characterized by keratinocyte hyperproliferation, inflammation, and aberrant differentiation. Imiquimod-induced psoriasis in rodent models has been widely used to study the pathogenesis of the disease and evaluate potential therapeutic interventions. In this study, we investigated the efficacy of two commonly used treatments, Clobetasol and Tacrolimus, in ameliorating psoriatic symptoms in an Imiquimod-induced psoriasis Wistar rat model. Interestingly, rat models are poorly evaluated in the literature despite rats displaying several advantages in evaluating pharmacological substances. Psoriasis-like skin lesions were induced by topical application of Imiquimod cream on shaved dorsal skin for seven consecutive days. Following induction, rats in the treatment groups received either a Clobetasol or Tacrolimus ointment once daily for one week, while the control group did not receive any application. Disease severity was assessed using clinical scoring, histological examination, and measurement of proinflammatory cytokine levels. Both Clobetasol and Tacrolimus treatments significantly reduced psoriatic lesion severity compared to the control group. Clinical scoring revealed a decrease in erythema, scaling, transepidermal water loss, and thickness of skin lesions in both treatment groups with a more marked effect with Clobetasol. Histological analysis demonstrated reduced epidermal hyperplasia in treated animals compared to controls. Furthermore, Clobetasol led to a significant reduction in the expression levels of the interleukin-17 (IL-17a and IL-17f) proinflammatory cytokines in lesioned skin. Overall, our findings demonstrated the therapeutic efficacy of both Clobetasol and, in a modest manner, Tacrolimus in attenuating Imiquimod-induced psoriasis-like symptoms in a rat model. These results support the clinical use of these agents in the management of psoriasis and mitigating psoriatic inflammation. They also provide insights into the use of rats as a relevant species for the Imiquimod-induced psoriasis model. Full article
(This article belongs to the Special Issue News in Skin Diseases: From Basic Mechanisms to Therapies)
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16 pages, 4308 KiB  
Article
The Role of TLR7 and TLR9 in the Pathogenesis of Systemic Sclerosis
by Chenyang Wang, Kyosuke Oishi, Tadahiro Kobayashi, Ko Fujii, Motoki Horii, Natsumi Fushida, Tasuku Kitano, Shintaro Maeda, Yuichi Ikawa, Akito Komuro, Yasuhito Hamaguchi and Takashi Matsushita
Int. J. Mol. Sci. 2024, 25(11), 6133; https://doi.org/10.3390/ijms25116133 - 1 Jun 2024
Cited by 1 | Viewed by 1468
Abstract
The bleomycin-induced scleroderma model is a well-established and dependable method for creating a mouse model of SSc (systemic sclerosis). In the field of skin connective tissue diseases, increasing evidence from clinical and animal experiments suggests that TLRs (Toll-like receptors) play an important role [...] Read more.
The bleomycin-induced scleroderma model is a well-established and dependable method for creating a mouse model of SSc (systemic sclerosis). In the field of skin connective tissue diseases, increasing evidence from clinical and animal experiments suggests that TLRs (Toll-like receptors) play an important role in several diseases. This study aimed to determine the role of TLR7 (Toll-like receptor 7) and TLR9 (Toll-like receptor 9) in the mechanisms of immune abnormalities and fibrosis in SSc. This study used TLR7-KO mice (TLR7-knockout mice with a balb/c background) and TLR9-KO mice (TLR9-knockout mice with a balb/c background) as well as WT mice (wild-type balb/c mice). All three kinds of mice were induced by BLM (bleomycin) in a scleroderma model as the experimental group; meanwhile, WT mice treated with PBS (phosphate-buffered saline) were used as the control group. We analyzed the fibrotic phenotype and the immunological abnormality phenotype of TLR7-deficient and TLR9-deficient mice in the SSc disease model using flow cytometry, RT-PCR (reverse transcription–polymerase chain reaction), a histological examination, and IHC (immunohistochemical staining). In a mouse model of SSc disease, the deletion of TLR7 attenuated skin and lung fibrosis, while the deletion of TLR9 exacerbated skin and lung fibrosis. The deletion of TLR7 resulted in a relative decrease in the infiltration and expression of various pro-inflammatory and fibrotic cells and cytokines in the skin. On the other hand, the deletion of TLR9 resulted in a relative increase in the infiltration and expression of various pro-inflammatory and cytokine-inhibiting cells and cytokines in the skin. Under the influence of pDCs (plasmacytoid dendritic cells), the balances of Beff/Breg (IL-6 + CD19 + B cell/IL-10 + CD19 + B cell), Th17/Treg (IL-17A + CD4 + T cell/Foxp3 + CD25 + CD4 + T cell), M1/M2 (CD86 + macrophage/CD206 + macrophage), and Th1/Th2 (TNFα + CD3 + CD4 + T cell/IL-4 + CD3 + CD4 + T cell) were biased towards the suppression of inflammation and fibrosis as a result of the TLR7 deletion. Comparatively, the balance was biased towards promoting inflammation and fibrosis due to the TLR9 deletion. In the SSc model, TLR7 promoted inflammation and fibrosis progression, while TLR9 played a protective role. These results suggest that TLR7 and TLR9 play opposite roles in triggering SSc to produce immune system abnormalities and skin fibrosis. Full article
(This article belongs to the Special Issue News in Skin Diseases: From Basic Mechanisms to Therapies)
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22 pages, 5296 KiB  
Article
Skin Anti-Inflammatory Potential with Reduced Side Effects of Novel Glucocorticoid Receptor Agonists
by Enrica Flori, Sarah Mosca, Daniela Kovacs, Stefania Briganti, Monica Ottaviani, Arianna Mastrofrancesco, Mauro Truglio and Mauro Picardo
Int. J. Mol. Sci. 2024, 25(1), 267; https://doi.org/10.3390/ijms25010267 - 23 Dec 2023
Cited by 2 | Viewed by 1463
Abstract
Glucocorticoids (GCs) are commonly used in the treatment of inflammatory skin diseases, although the balance between therapeutic benefits and side effects is still crucial in clinical practice. One of the major and well-known adverse effects of topical GCs is cutaneous atrophy, which seems [...] Read more.
Glucocorticoids (GCs) are commonly used in the treatment of inflammatory skin diseases, although the balance between therapeutic benefits and side effects is still crucial in clinical practice. One of the major and well-known adverse effects of topical GCs is cutaneous atrophy, which seems to be related to the activation of the glucorticoid receptor (GR) genomic pathway. Dissociating anti-inflammatory activity from atrophogenicity represents an important goal to achieve, in order to avoid side effects on keratinocytes and fibroblasts, known target cells of GC action. To this end, we evaluated the biological activity and safety profile of two novel chemical compounds, DE.303 and KL.202, developed as non-transcriptionally acting GR ligands. In primary keratinocytes, both compounds demonstrated anti-inflammatory properties inhibiting NF-κB activity, downregulating inflammatory cytokine release and interfering with pivotal signaling pathways involved in the inflammatory process. Of note, these beneficial actions were not associated with GC-related atrophic effects: treatments of primary keratinocytes and fibroblasts with DE.303 and KL.202 did not induce, contrarily to dexamethasone—a known potent GC—alterations in extracellular matrix components and lipid synthesis, thus confirming their safety profile. These data provide the basis for evaluating these compounds as effective alternatives to the currently used GCs in managing inflammatory skin diseases. Full article
(This article belongs to the Special Issue News in Skin Diseases: From Basic Mechanisms to Therapies)
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Review

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19 pages, 2292 KiB  
Review
The Skin–Brain Axis: From UV and Pigmentation to Behaviour Modulation
by Anna A. Ascsillán and Lajos V. Kemény
Int. J. Mol. Sci. 2024, 25(11), 6199; https://doi.org/10.3390/ijms25116199 - 4 Jun 2024
Cited by 3 | Viewed by 2155
Abstract
The skin–brain axis has been suggested to play a role in several pathophysiological conditions, including opioid addiction, Parkinson’s disease and many others. Recent evidence suggests that pathways regulating skin pigmentation may directly and indirectly regulate behaviour. Conversely, CNS-driven neural and hormonal responses have [...] Read more.
The skin–brain axis has been suggested to play a role in several pathophysiological conditions, including opioid addiction, Parkinson’s disease and many others. Recent evidence suggests that pathways regulating skin pigmentation may directly and indirectly regulate behaviour. Conversely, CNS-driven neural and hormonal responses have been demonstrated to regulate pigmentation, e.g., under stress. Additionally, due to the shared neuroectodermal origins of the melanocytes and neurons in the CNS, certain CNS diseases may be linked to pigmentation-related changes due to common regulators, e.g., MC1R variations. Furthermore, the HPA analogue of the skin connects skin pigmentation to the endocrine system, thereby allowing the skin to index possible hormonal abnormalities visibly. In this review, insight is provided into skin pigment production and neuromelanin synthesis in the brain and recent findings are summarised on how signalling pathways in the skin, with a particular focus on pigmentation, are interconnected with the central nervous system. Thus, this review may supply a better understanding of the mechanism of several skin–brain associations in health and disease. Full article
(This article belongs to the Special Issue News in Skin Diseases: From Basic Mechanisms to Therapies)
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