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Special Issue "Skin Inflammation Aging and 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: 28 February 2021.

Special Issue Editor

Dr. Serena Lembo
Website
Guest Editor
Università di Salerno, Salerno, Italy
Interests: photodermatology; inflammatory skin diseases

Special Issue Information

Dear Colleagues,

The skin is the most precious dress we wear every day.

It is the body's largest organ, with a complex structure made of several tissue layers, each with a distinct cellular composition. Its most important function is to form a “barrier” to protect our body from environmental insults. The skin is a high-turnover organ, with a continuously regenerating epidermis. With aging, both the epidermis and the dermis lose their regenerative ability, undergoing thinning, wrinkling, dryness, and mottling (intrinsic aging).

The inability to restore the integrity of the skin barrier can result in many cutaneous health problems such as inflammatory skin conditions.

In turn, chronic inflammation may enhance and speed aging.

Chronic exposure to environmental elements like ultraviolet (UV) radiations cause deleterious effects in skin cells; in fact, UVA and UVB radiation are associated with skin photo-aging, various inflammatory disorders, and also skin cancer (extrinsic aging). Research in recent years has advanced our understanding of the pathophysiology of inflammatory skin diseases and skin cancer, as well as of therapeutic options for skin aging. 

Nevertheless, many aspects remain to be explored: what is the role of the skin microenvironment in aging, inflammation, and cancer? Is there a link between skin aging, chronic inflammation, and skin cancer? Do they share molecular inflammatory pathways? Can we identify predictive biomarkers?

This Special Issue calls for original research papers, full reviews, and perspectives that address our current knowledge and progress in the field of skin inflammation, aging, and disease, to find possible answers to the mentioned questions and to others related to the keywords reported below.

Dr. Serena Lembo
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 papers will be 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

  • Skin health
  • Skin barrier
  • Inflammation Aging
  • Photoaging Intrinsic aging
  • Extrinsic aging
  • Skin cancer
  • Inflammatory skin conditions
  • Oxidative stress
  • Molecular inflammatory pathways

Published Papers (3 papers)

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Research

Open AccessArticle
Ameliorating Fibrotic Phenotypes of Keloid Dermal Fibroblasts through an Epidermal Growth Factor-Mediated Extracellular Matrix Remodeling
Int. J. Mol. Sci. 2021, 22(4), 2198; https://doi.org/10.3390/ijms22042198 - 23 Feb 2021
Abstract
Keloid and hypertrophic scars are skin fibrosis-associated disorders that exhibit an uncontrollable proliferation of fibroblasts and their subsequent contribution to the excessive accumulation of extracellular matrix (ECM) in the dermis. In this study, to elucidate the underlying mechanisms, we investigated the pivotal roles [...] Read more.
Keloid and hypertrophic scars are skin fibrosis-associated disorders that exhibit an uncontrollable proliferation of fibroblasts and their subsequent contribution to the excessive accumulation of extracellular matrix (ECM) in the dermis. In this study, to elucidate the underlying mechanisms, we investigated the pivotal roles of epidermal growth factor (EGF) in modulating fibrotic phenotypes of keloid and hypertrophic dermal fibroblasts. Our initial findings revealed the molecular signatures of keloid dermal fibroblasts and showed the highest degree of skin fibrosis markers, ECM remodeling, anabolic collagen-cross-linking enzymes, such as lysyl oxidase (LOX) and four LOX-like family enzymes, migration ability, and cell–matrix traction force, at cell–matrix interfaces. Furthermore, we observed significant EGF-mediated downregulation of anabolic collagen-cross-linking enzymes, resulting in amelioration of fibrotic phenotypes and a decrease in cell motility measured according to the cell–matrix traction force. These findings offer insight into the important roles of EGF-mediated cell–matrix interactions at the cell–matrix interface, as well as ECM remodeling. Furthermore, the results suggest their contribution to the reduction of fibrotic phenotypes in keloid dermal fibroblasts, which could lead to the development of therapeutic modalities to prevent or reduce scar tissue formation. Full article
(This article belongs to the Special Issue Skin Inflammation Aging and Diseases)
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Open AccessArticle
Increased Histone Acetylation and Decreased Expression of Specific Histone Deacetylases in Ultraviolet-Irradiated and Intrinsically Aged Human Skin In Vivo
Int. J. Mol. Sci. 2021, 22(4), 2032; https://doi.org/10.3390/ijms22042032 - 18 Feb 2021
Abstract
Histone deacetylases (HDACs) are conserved enzymes that remove acetyl groups from lysine side chains in histones and other proteins and play a crucial role in epigenetic regulation. Previously, we showed that histone acetylation is implicated in ultraviolet (UV)-induced inflammation and matrix impairment. To [...] Read more.
Histone deacetylases (HDACs) are conserved enzymes that remove acetyl groups from lysine side chains in histones and other proteins and play a crucial role in epigenetic regulation. Previously, we showed that histone acetylation is implicated in ultraviolet (UV)-induced inflammation and matrix impairment. To elucidate the histone acetylation status and specific HDACs involved in skin aging, we examined the changes in histone acetylation, global HDAC activity, and the expression of HDACs and sirtuins (SIRTs) in intrinsically aged and photoaged human skin as well as in UV-irradiated human skin in vivo. Following acute UV irradiation, the acetylated histone H3 (AcH3) level was increased, but HDAC activity and the expression levels of HDAC4, HDAC11, and SIRT4 were significantly decreased. In intrinsically aged skin, AcH3 levels were increased, but HDAC activity and the expression levels of HDAC4, HDAC5, HDAC10, HDAC11, SIRT6, and SIRT7 were significantly decreased. However, histone acetylation and HDAC expression in photoaged skin were not significantly different from those in intrinsically aged skin. Collectively, HDAC4 and HDAC11 were decreased in both UV-irradiated and intrinsically aged skin, suggesting that they may play a universal role in increased histone acetylation associated with skin aging. Full article
(This article belongs to the Special Issue Skin Inflammation Aging and Diseases)
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Open AccessArticle
UV-Induced Reduction of ACVR1C Decreases SREBP1 and ACC Expression by the Suppression of SMAD2 Phosphorylation in Normal Human Epidermal Keratinocytes
Int. J. Mol. Sci. 2021, 22(3), 1101; https://doi.org/10.3390/ijms22031101 - 22 Jan 2021
Abstract
Activin A receptor type 1C (ACVR1C), a type I transforming growth factor-β (TGF-β) receptor, has been implicated in sensitive skin and psoriasis and is involved in the regulation of metabolic homeostasis as well as cell proliferation and differentiation. In this study, we identified [...] Read more.
Activin A receptor type 1C (ACVR1C), a type I transforming growth factor-β (TGF-β) receptor, has been implicated in sensitive skin and psoriasis and is involved in the regulation of metabolic homeostasis as well as cell proliferation and differentiation. In this study, we identified a novel role of ACVR1C in the ultraviolet (UV)-irradiation-induced reduction of epidermal lipogenesis in human skin. UV irradiation decreased ACVR1C expression and epidermal triglyceride (TG) synthesis in human skin in vivo and in primary normal human epidermal keratinocytes (NHEK) in vitro. Lipogenic genes, including genes encoding acetyl-CoA carboxylase (ACC) and sterol regulatory element binding protein-1 (SREBP1), were significantly downregulated in UV-irradiated NHEK. ACVR1C knockdown by shRNA resulted in greater decreases in SREBP1 and ACC in response to UV irradiation. Conversely, the overexpression of ACVR1C attenuated the UV-induced decreases in SREBP1 and ACC. Further mechanistic study revealed that SMAD2 phosphorylation mediated the ACVR1C-induced lipogenic gene modulation. Taken together, a decrease in ACVR1C may cause UV-induced reductions in SREBP1 and ACC as well as epidermal TG synthesis via the suppression of SMAD2 phosphorylation. ACVR1C may be a target for preventing or treating UV-induced disruptions in lipid metabolism and associated skin disorders. Full article
(This article belongs to the Special Issue Skin Inflammation Aging and Diseases)
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