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Molecular Mechanisms and Therapeutic Targets in Skin Diseases
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Molecular Mechanisms and Therapeutic Targets in Skin Diseases

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: 30 November 2024 | Viewed by 4449

Special Issue Editor

Dr. Hanna Mys̈liwiec

E-Mail Website
Guest Editor
Department of Dermatology and Venereology, Medical University of Bialystok, 15-540 Bialystok, Poland
Interests: psoriasis; dermatology; skin disease; inflammation; aesthetic medicine

Special Issue Information

Dear Colleagues,

In recent decades, significant strides have been made in the development of novel therapeutic modalities for the treatment of various skin diseases, particularly within the realm of biologics. Despite these advancements, a deep comprehension of the molecular pathogenesis of numerous conditions remains imperative to pave the way for innovative therapeutic strategies.

Skin diseases can result from genetic predispositions, environmental factors, immune dysregulation, or a combination of these factors. By studying the molecular mechanisms involved in these diseases, researchers aim to unravel the intricate cellular processes contributing to their development, progression, and symptom manifestation. One of the paramount challenges in contemporary dermatology lies in the intricate interplay between skin diseases and comorbidities. Comprehensive investigations are warranted to elucidate these complex relationships and, subsequently, inform targeted therapeutic interventions.

In light of these critical areas, researchers and practitioners are encouraged to submit manuscripts covering, but not limited to, the following areas:

  • Molecular pathogenesis of skin diseases for the development of advanced therapeutic approaches.
  • The intricate connections between inflammatory skin lesions and systemic comorbidities.

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

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-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • inflammatory skin diseases
  • systemic inflammation
  • infectious skin diseases
  • comorbidity
  • pathogenesis
  • cytokines

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Published Papers (3 papers)

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Research

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13 pages, 2340 KiB  
Article
Difamilast, a Topical Phosphodiesterase 4 Inhibitor, Produces Soluble ST2 via the AHR–NRF2 Axis in Human Keratinocytes
by Gaku Tsuji, Ayako Yumine, Koji Kawamura, Masaki Takemura, Makiko Kido-Nakahara, Kazuhiko Yamamura and Takeshi Nakahara
Int. J. Mol. Sci. 2024, 25(14), 7910; https://doi.org/10.3390/ijms25147910 - 19 Jul 2024
Viewed by 1389
Abstract
Difamilast, a phosphodiesterase 4 (PDE4) inhibitor, has been shown to be effective in the treatment of atopic dermatitis (AD), although the mechanism involved remains unclear. Since IL-33 plays an important role in the pathogenesis of AD, we investigated the effect of difamilast on [...] Read more.
Difamilast, a phosphodiesterase 4 (PDE4) inhibitor, has been shown to be effective in the treatment of atopic dermatitis (AD), although the mechanism involved remains unclear. Since IL-33 plays an important role in the pathogenesis of AD, we investigated the effect of difamilast on IL-33 activity. Since an in vitro model of cultured normal human epidermal keratinocytes (NHEKs) has been utilized to evaluate the pharmacological potential of adjunctive treatment of AD, we treated NHEKs with difamilast and analyzed the expression of the suppression of tumorigenicity 2 protein (ST2), an IL-33 receptor with transmembrane (ST2L) and soluble (sST2) isoforms. Difamilast treatment increased mRNA and protein levels of sST2, a decoy receptor suppressing IL-33 signal transduction, without affecting ST2L expression. Furthermore, supernatants from difamilast-treated NHEKs inhibited IL-33-induced upregulation of TNF-α, IL-5, and IL-13 in KU812 cells, a basophil cell line sensitive to IL-33. We also found that difamilast activated the aryl hydrocarbon receptor (AHR)–nuclear factor erythroid 2-related factor 2 (NRF2) axis. Additionally, the knockdown of AHR or NRF2 abolished the difamilast-induced sST2 production. These results indicate that difamilast treatment produces sST2 via the AHR–NRF2 axis, contributing to improving AD symptoms by inhibiting IL-33 activity. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targets in Skin Diseases)
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Review

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9 pages, 905 KiB  
Review
The Carcinogenesis of the Human Scalp: An Immunometabolic-Centered View
by Baruch Kaplan, Rebecca von Dannecker and Jack L. Arbiser
Int. J. Mol. Sci. 2024, 25(22), 12064; https://doi.org/10.3390/ijms252212064 - 10 Nov 2024
Viewed by 415
Abstract
The human scalp is a common site of skin cancer in humans, with nonmelanoma skin cancer being exceedingly common. In this review, two dermatologists with extensive experience in cutaneous oncology will discuss unique features of the epidemiology of cancer of the scalp. Clinical [...] Read more.
The human scalp is a common site of skin cancer in humans, with nonmelanoma skin cancer being exceedingly common. In this review, two dermatologists with extensive experience in cutaneous oncology will discuss unique features of the epidemiology of cancer of the scalp. Clinical observations on these common skin cancers lead to insight into the pathogenesis and potential prevention and treatment of cutaneous scalp neoplasia. Our hypothesis is that the presence of hair protects against the development of skin cancer but not by serving as a physical shield but rather by providing continuous IL-17-biased immunosurveillance. The loss of hair allows for a release from immunosurveillance, resulting in the expansion of neoplastic cells towards skin cancer. Both hair follicles and metabolic changes in stroma allow for permissiveness for tumor promotion. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targets in Skin Diseases)
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21 pages, 2018 KiB  
Review
The Association between Genetics and Response to Treatment with Biologics in Patients with Psoriasis, Psoriatic Arthritis, Rheumatoid Arthritis, and Inflammatory Bowel Diseases: A Systematic Review and Meta-Analysis
by Rownaq Fares Al-Sofi, Mie Siewertsen Bergmann, Claus Henrik Nielsen, Vibeke Andersen, Lone Skov and Nikolai Loft
Int. J. Mol. Sci. 2024, 25(11), 5793; https://doi.org/10.3390/ijms25115793 - 26 May 2024
Viewed by 1965
Abstract
Genetic biomarkers could potentially lower the risk of treatment failure in chronic inflammatory diseases (CID) like psoriasis, psoriatic arthritis (PsA), rheumatoid arthritis (RA), and inflammatory bowel disease (IBD). We performed a systematic review and meta-analysis assessing the association between single nucleotide polymorphisms (SNPs) [...] Read more.
Genetic biomarkers could potentially lower the risk of treatment failure in chronic inflammatory diseases (CID) like psoriasis, psoriatic arthritis (PsA), rheumatoid arthritis (RA), and inflammatory bowel disease (IBD). We performed a systematic review and meta-analysis assessing the association between single nucleotide polymorphisms (SNPs) and response to biologics. Odds ratio (OR) with 95% confidence interval (CI) meta-analyses were performed. In total, 185 studies examining 62,774 individuals were included. For the diseases combined, the minor allele of MYD88 (rs7744) was associated with good response to TNFi (OR: 1.24 [1.02–1.51], 6 studies, 3158 patients with psoriasis or RA) and the minor alleles of NLRP3 (rs4612666) (OR: 0.71 [0.58–0.87], 5 studies, 3819 patients with RA or IBD), TNF-308 (rs1800629) (OR: 0.71 [0.55–0.92], 25 studies, 4341 patients with psoriasis, RA, or IBD), FCGR3A (rs396991) (OR: 0.77 [0.65–0.93], 18 studies, 2562 patients with psoriasis, PsA, RA, or IBD), and TNF-238 (rs361525) (OR: 0.57 [0.34–0.96]), 7 studies, 818 patients with psoriasis, RA, or IBD) were associated with poor response to TNFi together or infliximab alone. Genetic variants in TNFα, NLRP3, MYD88, and FcRγ genes are associated with response to TNFi across several inflammatory diseases. Most other genetic variants associated with response were observed in a few studies, and further validation is needed. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Therapeutic Targets in Skin Diseases)
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