The phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway regulates cell proliferation, differentiation, and migration, along with angiogenesis and metabolism. Additionally, it could mediate skin development and homeostasis. There is much evidence to suggest that dysregulation of PI3K/Akt pathway is frequently associated with several human cutaneous malignancies like malignant melanoma (MM), basal cell carcinoma (BCC), and cutaneous squamous cell carcinoma (SCC), as well as their poor outcomes. Nevertheless, emerging roles of PI3K/Akt pathway cascade in a group of common non-malignant skin disorders including acne and psoriasis, among others, have been recognized. The enhanced understanding of dysfunction of PI3K/Akt pathway in patients with these non-malignant disorders has offered a solid foundation for the progress of updated therapeutic targets. This article reviews the latest advances in the roles of PI3K/Akt pathway and their targets in the skin homeostasis and progression of a wide range of non-malignant skin disorders and describes the current progress in preclinical and clinical researches on the involvement of PI3K/Akt pathway targeted therapies.

Background: Over the last several decades, our understanding of hidradenitis suppurativa (HS) has improved considerably, thereby enhancing our ability to clinically diagnose and treat the disease.Objective: The purpose of this study was to identify and analyze the top 100 most-cited publications related to HS to update bibliometric information on HS.Materials and methods: We used the Web of Science database to identify reports on hidradenitis suppurativa. Data from the 100 most-cited publications were extracted and analyzed.Results: The citation number of the top 100 most-cited articles was 89–532 (mean, 153.51), with the most productive periods being from years 2007 to 2016. Most publications originated from the British Journal of Dermatology and the Journal of the American Academy of Dermatology. The 100 articles originated from 18 countries, with Denmark being the most productive country, followed by the United States (17), England (14), and Germany (12). Jemec GB, from the University of Copenhagen, had 32 citations and was the most frequently identified author. The 100 articles encompassed several fields of research as follows: pathogenesis (18%), pathophysiology (7%), epidemiology (14%), clinical diagnosis and features (16%), treatment (25%), comorbidity (10%), and others (10%). In total, 11 reviews, three guidelines, and 86 original articles (nine randomized clinical trials) were included.Conclusion: Through this bibliometric analysis, we aimed to indicate a series of intellectual landmark publications that offer us critical reviews, guidelines, and original articles, which highlight the immense level of progress achieved in the field of HS.

Background. Chronic cutaneous lupus erythematosus (CCLE) and subacute cutaneous lupus erythematosus (SCLE) are both common variants of cutaneous lupus erythematosus (CLE) that mainly involve the skin and mucous membrane. Oral mucosal involvement is frequently observed in patients of CLE. Despite that they have different clinicopathological features, whether there is a significant difference in pathogenesis between them remains unclear. Herein, we investigated specific genes and pathways of SCLE and CCLE via bioinformatics analysis. Methods. Microarray expression datasets of GSE109248 and GSE112943 were both retrieved from the GEO database. Differentially expressed genes (DEGs) between CCLE or SCLE skin tissues and health controls were selected by GEO2R. Common DEGs were picked out via the Venn diagram software. Then, functional enrichment and PPI network analysis were conducted, and the top 10 key genes were identified via Cytohubba. Results. Totally, 176 DEGs of SCLE and 287 DEGs of CCLE were identified. The GO enrichment and KEGG analysis of DEGs of SCLE is significantly enriched in the response to virus, defense response to virus, response to IFN-gamma, cellular response to IFN-γ, type I IFN signaling pathway, chemokine activity, chemokine receptor binding, NOD-like receptor signaling pathway, etc. The GO enrichment and KEGG analysis of DEGs of CCLE is significantly enriched in the response to virus, regulation of multiorganism process, negative regulation of viral process, regulation of lymphocyte activation, chemokine receptor binding, CCR chemokine receptor binding, NOD-like receptor signaling pathway, etc. The top 10 hub genes of SCLE and CCLE, respectively, include STAT1, CXCL10, IRF7, ISG15, and RSAD2 and CXCL10, IRF7, IFIT3, CTLA4, and ISG15. Conclusion. Our finding suggests that SCLE and CCLE have the similar potential key genes and pathways and majority of them belong to IFN signatures and IFN signaling pathway. Besides, the NOD-like receptor signaling pathway might also have an essential role in the pathogenesis of SCLE and CCLE. Together, the identified genes and signaling pathways have enhanced our understanding of the mechanism underlying the occurrence and development of both SCLE and CCLE.