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Advances of Skin Disease
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Advances of Skin Disease

A special issue of Journal of Personalized Medicine (ISSN 2075-4426). This special issue belongs to the section "Mechanisms of Diseases".

Deadline for manuscript submissions: closed (10 May 2023) | Viewed by 5370

Special Issue Editor

Dr. Jorge Feito

E-Mail Website
Guest Editor
Pathology Department, Complejo Asistencial Universitario de Salamanca, 37007 Salamanca, Spain
Interests: dermatopathology; mechanoreception; sensory corpuscles; peripheral nervous system; digestive pathology

Special Issue Information

Dear Colleagues,

The skin represents the most exposed barrier of organisms, and, as such, has been the subject of intensive research focused on both neoplastic and inflammatory conditions. Recently, personalized therapies have gained attention not only on the scientific level, but also on the clinical level. These therapies have revolutionized oncology, with melanoma being the most explored cutaneous disease, by the use of new, cutting-edge treatments, including immunotherapies and targeted therapies. Personalized therapies are not limited to oncologic diseases, as much interest has been put into detecting and applying biological agents in several inflammatory disorders. As a superficial barrier, the skin has also received notable interest regarding its drug administration capacities. Moreover, research even has to consider the essential role of the skin in increasingly valued aesthetics, not only as a primary need of patients but also in avoiding side effects.

This proposed Special Issue aims to collect the most recent insights into clinical and translational research regarding melanoma, nonmelanoma skin neoplasms, and inflammatory cutaneous conditions. The scope of the research includes studies with novel diagnostic or therapeutic approaches that can result in more personalized and efficient cutaneous medicine, including molecular/cellular mechanisms, detection, stratification, surveillance, care management, or treatment of cutaneous diseases. 

Dr. Jorge Feito
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. Journal of Personalized Medicine 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 2600 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

  • cutaneous melanoma
  • superficial epithelium tumors
  • connective tissue tumors
  • cutaneous lymphoma
  • inflammatory diseases of subcutaneous fat
  • lichenoid dermatitis
  • psoriasiform dermatosis
  • acantholytic and blistering disorders

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

11 pages, 1725 KiB  
Article
The Associations of Single Nucleotide Polymorphisms of the COL3A1, COL6A5, and COL8A1 Genes with Atopic Dermatitis
by Krzysztof Szalus, Weronika Zysk, Jolanta Gleń, Monika Zabłotna, Roman J. Nowicki and Magdalena Trzeciak
J. Pers. Med. 2023, 13(4), 661; https://doi.org/10.3390/jpm13040661 - 13 Apr 2023
Cited by 5 | Viewed by 2032
Abstract
The pathophysiology of atopic dermatitis (AD) is complex, multifactorial, and not fully understood. Genes encoding collagens, the most abundant proteins in the extracellular matrix (ECM), may play a potential role in the pathogenesis of AD. Our study aimed to estimate the associations between [...] Read more.
The pathophysiology of atopic dermatitis (AD) is complex, multifactorial, and not fully understood. Genes encoding collagens, the most abundant proteins in the extracellular matrix (ECM), may play a potential role in the pathogenesis of AD. Our study aimed to estimate the associations between Col3A1/rs1800255, Col6A5 /29rs12488457, and Col8A1/rs13081855 polymorphisms and the occurrence, course, and features of AD in the Polish population. Blood samples were collected from 157 patients with AD and 111 healthy volunteers. The genotype distribution of the investigated collagens genes did not differ significantly between the AD and control subjects (p > 0.05). The AA genotype of Col3A1/rs1800255 was significantly associated with the occurrence of mild SCORAD (OR = 0.16; 95% Cl: 0.03–0.78; p = 0.02) and mild pruritus (OR = 18.5; 95% Cl: 3.48–98.40; p = 0.0006), while the GG genotype was significantly associated with severe SCORAD (OR = 6.6; 95% Cl: 1.23–32.35; p = 0.03). Regarding Col6A5/29rs12488457 polymorphism, the average SCORAD score was significantly lower in the group of patients with genotype AA than in patients with the AC genotype (39.8 vs. 53.4; p = 0.04). Nevertheless, both average SCORAD scores were high, and represent the moderate and severe grades of the diseases, respectively. The single nucleotide polymorphisms (SNPs) of COL3A1/ rs1800255 and Col6A5/29rs12488457 seem to be associated with AD courses and symptoms, suggesting new disease biomarkers. The modulation of collagens, the major component of the ECM, may serve as a therapeutic target of AD in the future. Full article
(This article belongs to the Special Issue Advances of Skin Disease)
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15 pages, 3596 KiB  
Article
Severe Burn Injury Significantly Alters the Gene Expression and m6A Methylation Tagging of mRNAs and lncRNAs in Human Skin
by Yanqin Ran, Zhuoxian Yan, Mitao Huang, Situo Zhou, Fangqin Wu, Mengna Wang, Sifan Yang, Pihong Zhang, Xiaoyuan Huang, Bimei Jiang and Pengfei Liang
J. Pers. Med. 2023, 13(1), 150; https://doi.org/10.3390/jpm13010150 - 12 Jan 2023
Cited by 7 | Viewed by 2746
Abstract
N6-methyladenosine (m6A) modulates RNA metabolism and functions in cell differentiation, tissue development, and immune response. After acute burns, skin wounds are highly susceptible to infection and poor healing. However, our understanding of the effect of burn injuries on m6A methylation and their potential [...] Read more.
N6-methyladenosine (m6A) modulates RNA metabolism and functions in cell differentiation, tissue development, and immune response. After acute burns, skin wounds are highly susceptible to infection and poor healing. However, our understanding of the effect of burn injuries on m6A methylation and their potential mechanism is still limited. Human m6A-mRNA&lncRNA Epitranscriptomic microarray was used to obtain comprehensive mRNA and lncRNA transcriptome m6A profiling and gene expression patterns after burn injuries in human skin tissue. Bioinformatic and functional analyses were conducted to find molecular functions. Microarray profiling showed that 65 mRNAs and 39 lncRNAs were significantly hypermethylated; 5492 mRNAs and 754 lncRNAs were significantly hypomethylated. Notably, 3989 hypomethylated mRNAs were down-expressed and inhibited many wound healing biological processes and pathways including in the protein catabolic process and supramolecular fiber organization pathway; 39 hypermethylated mRNAs were up-expressed and influenced the cell surface receptor signaling pathway and inflammatory response. Moreover, we validated that m6A regulators (METTL14, METTL16, ALKBH5, FMR1, and HNRNPC) were significantly downregulated after burn injury which may be responsible for the alteration of m6A modification and gene expression. In summary, we found that homeostasis in the skin was disrupted and m6A modification may be a potential mechanism affecting trauma infection and wound healing. Full article
(This article belongs to the Special Issue Advances of Skin Disease)
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