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New Insights into the Use of Mouse Models for the Study of Skin Disorders

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: closed (20 June 2025) | Viewed by 4096

Special Issue Editor

Dr. Jing Feng

E-Mail Website
Guest Editor
Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China
Interests: mouse models; skin disorders; epithelia; sensory nerve; immune cell; ion channel; GPCR; cytokines; neurotransmitters

Special Issue Information

Dear Colleagues,

The skin is the largest organ of the body. The skin and its derivatives (hair, nails, sweat and oil glands), as well as numerous cell types (epithelial keratinocytes, innate and adaptive immune cells, melanocytes, and sensory nerves), make up the integumentary system, which maintains the skin barrier, interplays between the host and the external environment and protects the body from external nocious stimuli. Although recent studies have begun to elucidate the molecular, cellular and signling pathways that underlie physiological functions and the development of pathological conditions in the skin, the lack of critical mouse models for mechanistical studies has severely limited the development of new therapies for effectively treating skin disorders. In this Special Issue, we invite authors to submit original research and review articles that will contribute to a better understanding of the following topics: newly developed mouse models of various skin disorders, skin lesions, skin cancer, sensory disorders (pain and itch), sensitive skin, immune disregulation in the skin, skin infection, skin neuroendocrinology, skin hypertrophy and skin pigmentation.

Dr. Jing Feng
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

  • pain
  • itch
  • inflammation
  • endocrine
  • infection
  • hypertrophy
  • aging
  • hair loss
  • wound healing

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Published Papers (3 papers)

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Research

19 pages, 6166 KB  
Article
Deletion of the Epidermal Protease KLK5 Aggravates the Symptoms of Congenital Ichthyosis CDSN-nEDD
by Eleni Zingkou, Marie Reynier, Georgios Pampalakis, Guy Serre, Nathalie Jonca and Georgia Sotiropoulou
Int. J. Mol. Sci. 2025, 26(17), 8605; https://doi.org/10.3390/ijms26178605 - 4 Sep 2025
Viewed by 475
Abstract
Congenital ichthyoses, now grouped under the acronym EDD (Epidermal Differentiation Disorders), include nonsyndromic forms (nEDD) that may be caused by loss-of-function mutations in the CDSN gene encoding corneodesmosin (CDSN-nEDD, formerly Peeling skin syndrome type 1). It is characterized by skin peeling, [...] Read more.
Congenital ichthyoses, now grouped under the acronym EDD (Epidermal Differentiation Disorders), include nonsyndromic forms (nEDD) that may be caused by loss-of-function mutations in the CDSN gene encoding corneodesmosin (CDSN-nEDD, formerly Peeling skin syndrome type 1). It is characterized by skin peeling, inflammation, itching and food allergies, while no specific therapy is currently available. High levels of KLK5, the serine protease that initiates the desquamation cascade, are found in the epidermis of CDSN-nEDD patients. Thus, we hypothesized that KLK5 inhibition would alleviate the symptoms of CDSN-nEDD and could serve as a new pharmacological target. A human epidermal equivalent (HEE) model for CDSN-nEDD was developed using shRNA-mediated CDSN knockdown. This model was characterized and used to assess the role of KLK5 knockdown on CDSN-nEDD. Also, Klk5−/− mice were crossed with Cdsnepi−/− mice, the murine model of CDSN-nEDD, to examine in vivo the effect(s) of Klk5 deletion in CDSN-nEDD. Both models recapitulated the CDSN-nEDD desquamating phenotype. Elimination of KLK5 aggravated the CDSN-nEDD phenotype. Epidermal proteolysis was surprisingly elevated, while severe ultrastructural (corneo)desmosomal alterations increased epidermal barrier permeability and stratum corneum detachment was manifested. Based on these results, we concluded that targeting epidermal proteolysis with KLK5 ablation cannot compensate for the loss of corneodesmosin and rescue over-desquamation of the CDSN-nEDD. Possibly, in the absence of KLK5, other proteases take over which increases the severity of over-desquamation in CDSN-nEDD. The translational outcome is that over-desquamation may not always be rescued by eliminating epidermal proteolysis, but fine protease modulation is more likely required. Full article
(This article belongs to the Special Issue New Insights into the Use of Mouse Models for the Study of Skin Disorders)
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20 pages, 12622 KB  
Article
Paw Skin as a Translational Model for Investigating Fibrotic and Inflammatory Wound Healing Defects in Recessive Dystrophic Epidermolysis Bullosa
by Cristian De Gregorio, Giselle Ramos-Gonzalez, Bernardo Morales-Catalán, Fernando Ezquer and Marcelo Ezquer
Int. J. Mol. Sci. 2025, 26(9), 4281; https://doi.org/10.3390/ijms26094281 - 30 Apr 2025
Cited by 1 | Viewed by 770
Abstract
Recessive dystrophic epidermolysis bullosa (RDEB) is a severe genetic disease caused by COL7A1 mutations. It leads to skin fragility, chronic inflammation, and impaired wound healing. The condition often results in fibrotic scarring, pseudosyndactyly, and cutaneous squamous cell carcinoma (SCC). However, current animal models [...] Read more.
Recessive dystrophic epidermolysis bullosa (RDEB) is a severe genetic disease caused by COL7A1 mutations. It leads to skin fragility, chronic inflammation, and impaired wound healing. The condition often results in fibrotic scarring, pseudosyndactyly, and cutaneous squamous cell carcinoma (SCC). However, current animal models fail to fully replicate chronic RDEB wounds. In this study, we used Collagen VII-hypomorphic mice (Col7a1flNeo/flNeo) and created full-thickness wounds on their paw skin, an area prone to fibrosis due to mechanical stress. We analyzed the healing process using histology, immunofluorescence, and electron microscopy. The RDEB mice showed delayed wound closure, increased inflammation, and poor granulation tissue formation. At 30 days post-injury, we observed persistent fibrosis, with elevated levels of Collagen I, α-SMA+ myofibroblasts, and tenascin-C. These mice also had fewer intraepidermal nerve fibers, which may help explain the neuropathic pain associated with RDEB. Our model reproduces the main features of chronic RDEB wounds. It offers a useful tool for evaluating therapies aimed at reducing inflammation, fibrosis, and tumor risk in these patients. Full article
(This article belongs to the Special Issue New Insights into the Use of Mouse Models for the Study of Skin Disorders)
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16 pages, 2916 KB  
Article
Chronic Morphine Treatment and Antiretroviral Therapy Exacerbate HIV-Distal Sensory Peripheral Neuropathy and Induce Distinct Microbial Alterations in the HIV Tg26 Mouse Model
by Danielle Antoine, Irina Chupikova, Richa Jalodia, Praveen Kumar Singh and Sabita Roy
Int. J. Mol. Sci. 2024, 25(3), 1569; https://doi.org/10.3390/ijms25031569 - 26 Jan 2024
Cited by 4 | Viewed by 2097
Abstract
Distal Sensory Peripheral Neuropathy (DSP) is a common complication in HIV-infected individuals, leading to chronic pain and reduced quality of life. Even with antiretroviral therapy (ART), DSP persists, often prompting the use of opioid analgesics, which can paradoxically worsen symptoms through opioid-induced microbial [...] Read more.
Distal Sensory Peripheral Neuropathy (DSP) is a common complication in HIV-infected individuals, leading to chronic pain and reduced quality of life. Even with antiretroviral therapy (ART), DSP persists, often prompting the use of opioid analgesics, which can paradoxically worsen symptoms through opioid-induced microbial dysbiosis. This study employs the HIV Tg26 mouse model to investigate HIV-DSP development and assess gut microbiome changes in response to chronic morphine treatment and ART using 16S rRNA sequencing. Our results reveal that chronic morphine and ART exacerbate HIV-DSP in Tg26 mice, primarily through mechanical pain pathways. As the gut microbiome may be involved in chronic pain persistence, microbiome analysis indicated distinct bacterial community changes between WT and Tg26 mice as well as morphine- and ART-induced microbial changes in the Tg26 mice. This study reveals the Tg26 mouse model to be a relevant system that can help elucidate the pathogenic mechanisms of the opioid- and ART-induced exacerbation of HIV-associated pain. Our results shed light on the intricate interplay between HIV infection, ART, opioid use, and the gut microbiome in chronic pain development. They hold implications for understanding the mechanisms underlying HIV-associated pain and microbial dysbiosis, with potential for future research focused on prevention and treatment strategies. Full article
(This article belongs to the Special Issue New Insights into the Use of Mouse Models for the Study of Skin Disorders)
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