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Skin Diseases: From Molecular Pathology to Novel Therapeutic Approaches

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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 June 2025 | Viewed by 6039

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Dr. Alicja Forma

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Department of Forensic Medicine, Medical University of Lublin, ul. Jaczewskiego 8b, 20-090 Lublin, Poland
Interests: metallomics; micronutrients; macronutrients; toxicology; environmental pollution; carcinogenesis
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Dear Colleagues,

Skin is the largest organ of the human body. It acts as the first line of defense against various environmental factors. A combination of those external factors, along with internal factors, induces a plethora of events that might disturb skin homeostasis, eventually leading to various diseases. A comprehensive understanding of the molecular basis of skin physiology and biochemistry not only provides insight into the processes that maintain skin health but also indicates the pathways through which the disease might occur. This eventually indicates the potential points which can be targeted while taking into account novel therapeutic approaches. Biological target research is of great importance for providing improved topical and oral skin disease treatment. For this Special Issue, we would like to invite you to submit papers concerning the pathology of the skin as well as new and pioneering treatment options and therapeutic strategies. We welcome the submission of original research articles, systematic and narrative reviews, meta-analyses, clinical trials, and case reports and commentaries.

Dr. Alicja Forma
Guest Editor

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Keywords

skin physiology and pathology
skin cancer
autoimmune skin diseases
microbial infections of skin
sexually transmitted diseases
molecular pathology
therapeutic advancements

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Published Papers (4 papers)

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Research

21 pages, 3483 KiB

Open AccessArticle

High Copy Number Variations Correlate with a Pro-Tumoral Microenvironment and Worse Prognosis in Acral Lentiginous Melanoma

by Inés de la Rosa, Pol Sisó, Christopher Ríos, Judith Gracia, Dolors Cuevas, Oscar Maiques, Núria Eritja, Xavier Soria, Joan Angel-Baldó, Sonia Gatius, Lidia Sanchez-Moral, Maria-Rosa Sarrias, Xavier Matias-Guiu, Rosa M. Martí and Anna Macià

Int. J. Mol. Sci. 2025, 26(9), 4097; https://doi.org/10.3390/ijms26094097 - 25 Apr 2025

Viewed by 71

Abstract

Acral lentiginous melanoma (ALM) is a rare melanoma subtype primarily located in acral regions. However, ALMs exhibit a distinctive genetic profile characterized by a high number of copy number variations (CNVs) and limited point mutations. Late diagnosis and restricted therapeutic efficacy contribute to its poor prognosis. The secretome within the tumor microenvironment (TME) influences immune modulation and plays a vital role in melanoma progression. We aim to analyze the role of ALM secretome and CNVs profile with prognosis in primary ALM patients. Here, we demonstrated that high CNV burden (CNVsHigh) was associated with worse clinicopathological characteristics and poor prognosis. Furthermore, our study also revealed that conditioned media (CM) of CNVsHigh genetic profile ALM cell line was associated with pro-tumoral, pro-angiogenic, and immunosuppressive secretome profiles. In addition, CM of CNVsHigh cell lines in vitro promotes macrophage polarization to immunosuppressive phenotype. Moreover, we observed an increased presence of immunosuppressive tumor-associated macrophages (TAMs) at the invasive front (IF) of CNVsHigh ALM biopsies. This research reveals the adverse prognostic impact of CNVsHigh in ALM patients, establishing a novel link with a pro-tumor secretome, offering potential biomarkers for prognosis and personalized treatment to enhanced disease monitoring in ALM patients. Full article

(This article belongs to the Special Issue Skin Diseases: From Molecular Pathology to Novel Therapeutic Approaches)

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13 pages, 832 KiB

Open AccessArticle

Biomarkers of Extracellular Matrix Fragments in Patients with Psoriasis

by Mila Broby Johansen, Signe Holm Nielsen, Helena Port, Tanja Todberg, Marianne Bengtson Løvendorf and Lone Skov

Int. J. Mol. Sci. 2025, 26(1), 261; https://doi.org/10.3390/ijms26010261 - 30 Dec 2024

Viewed by 1033

Abstract

Blood-based extracellular matrix (ECM) fragments have been identified as potential pharmacologic biomarkers in spondyloarthritis and diagnostic biomarkers in psoriatic arthritis and psoriasis vulgaris. This study aimed to explore whether ECM fragments can differentiate patients with psoriasis from healthy controls (HC) and determine their potential as biomarkers for response to treatment in psoriasis. The study population included 59 patients with moderate to severe psoriasis, not receiving systemic anti-psoriatic treatment at inclusion, and 52 HC matched by age, sex, and BMI. An EDTA plasma sample was taken from all subjects at inclusion. Nine patients with psoriasis who initiated treatment with adalimumab after inclusion and responded successfully had an additional EDTA plasma sample taken after three to six months. Twelve ECM fragments were measured using validated ELISAs and Immunodiagnostic Systems automated chemiluminescent assays. C4M, indicating collagen IV degradation, PRO-C3, indicating tissue fibrosis, and PRO-C4, indicating epidermal basement membrane turnover showed significantly elevated levels in psoriasis patients compared with HC (p = 0.005, p = 0.016, and p = 0.018, respectively). Despite successful treatment, adalimumab did not alter C4M, PRO-C3, or PRO-C4 levels. In conclusion, compared with controls, C4M, PRO-C3, and PRO-C4 were elevated in psoriasispatients, but treatment did not modulate these fragments. Full article

(This article belongs to the Special Issue Skin Diseases: From Molecular Pathology to Novel Therapeutic Approaches)

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14 pages, 4134 KiB

Open AccessArticle

Rosmarinic Acid Ameliorates Dermatophagoides farinae Extract-Induced Atopic Dermatitis-like Skin Inflammation by Activating the Nrf2/HO-1 Signaling Pathway

by Ki-Shuk Shim, Hye Jin Kim, Kon-Young Ji, Dong Ho Jung, Sun Haeng Park, Hyun-Kyung Song, Taesoo Kim and Ki Mo Kim

Int. J. Mol. Sci. 2024, 25(23), 12737; https://doi.org/10.3390/ijms252312737 - 27 Nov 2024

Cited by 2 | Viewed by 1064

Abstract

Atopic dermatitis (AD) is one of the most common chronic inflammatory skin diseases. AD pathogenesis is associated with increased oxidative stress, impairment of the skin barrier, and activation of the immune response. Rosmarinic acid (RA), a caffeic acid ester, is known for its anti-inflammatory and antioxidant properties. However, the effects of RA on Dermatophagoides farinae extract (DfE)-induced AD-like skin inflammation, as well as its ability to regulate oxidative stress through the Nrf2/HO-1 pathway in TNF-α/IFN-γ-treated keratinocytes, remain unclear. We investigated RA activity in a DfE-induced AD-like skin inflammation mouse model and IFN-γ/TNF-α-stimulated keratinocytes. We found that RA attenuates DfE-induced inflammation by decreasing dermatitis scores and serum inflammatory marker levels and mast cell infiltration. Additionally, RA significantly suppressed IFN-γ/TNF-α-induced chemokine production in keratinocytes and reduced Th cytokine levels in concanavalin A-stimulated splenocytes. Importantly, RA also increased Nrf2/HO-1 expression in TNF-α/IFN-γ-treated keratinocytes. In conclusion, this study demonstrated that RA effectively alleviates DfE-induced AD-like skin lesions by reducing the levels of inflammatory cytokines and chemokines. Furthermore, RA promotes Nrf2/HO-1 signaling in keratinocytes, which may help mitigate DfE-induced oxidative stress, thereby alleviating AD-like skin inflammation. These findings highlight the potential of RA as a therapeutic agent for treating AD and other skin inflammation. Full article

(This article belongs to the Special Issue Skin Diseases: From Molecular Pathology to Novel Therapeutic Approaches)

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14 pages, 4413 KiB

Open AccessArticle

TRPA1 Influences Staphylococcus aureus Skin Infection in Mice and Associates with HIF-1a and MAPK Pathway Modulation

by Manoj Yadav, Prem Prashant Chaudhary, Grace Ratley, Brandon D’Souza, Mahaldeep Kaur, Sundar Ganesan, Juraj Kabat and Ian A. Myles

Int. J. Mol. Sci. 2024, 25(18), 9933; https://doi.org/10.3390/ijms25189933 - 14 Sep 2024

Cited by 1 | Viewed by 1726

Abstract

Infections caused by methicillin-resistant Staphylococcus aureus (MRSA) are a major public health burden. Emerging antibiotic resistance has heightened the need for new treatment approaches for MRSA infection such as developing novel antimicrobial agents and enhancing the host’s defense response. The thermo-ion channels Transient Receptor Potential (TRP-) A1 and V1 have been identified as modulators of S. aureus quorum sensing in cell culture models. However, their effects on in vivo infection control are unknown. In this study, we investigated the therapeutic effect of natural TRP ion channel inhibitors on MRSA skin infection in mice. While deletion of TRPV1 did not affect lesion size or inflammatory markers, TRPA1^−/− mice demonstrated significantly reduced infection severity and abscess size. Treatment with natural inhibitors of TRPA1 with or without blockade of TRPV1 also reduced abscess size. Tissue transcriptomic data coupled with immunohistochemistry revealed that TRPA1 inhibition impacted heat shock protein expression (HSP), modulated the HIF-1a and MAPK pathways, and reduced IL4 expression. Additionally, metabolomics data showed an impact on purine and glycosaminoglycan pathways. Multi-omic integration of transcriptomic and metabolic data revealed that diacylglycerol metabolism was the likely bridge between metabolic and immunological impacts. Our findings suggest that TRPA1 antagonism could provide a promising and cost-effective therapeutic approach for reducing the severity of MRSA infection, and presents a novel underlying molecular mechanism. Full article

(This article belongs to the Special Issue Skin Diseases: From Molecular Pathology to Novel Therapeutic Approaches)

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