Mapping the evolution of acne research based on 100 top-cited articles: A bibliometric analysis of trends and hotspots from 2014 to 2023.

BACKGROUND: Acne is a prevalent inflammatory condition of the pilosebaceous unit, which seriously affects the appearance and mental health of patients. Bibliometrics is the statistical analysis of academic literature in a certain field. We aimed to characterize the 100 most cited articles on acne from a bibliometric perspective, as well as explore the frontier hotspots and trends of acne. METHODS: A search was conducted on the Web of Science database on August 8, 2023. we employed the terms "acne," "acne Vulgaris," and "common acne" in our search. The top 100 articles with the most citations throughout the time frame of 2014 to 2023 were discovered and assessed. The visualization study was carried out using bibliometric tools such as CiteSpace 6.2.R4, VOSviewer 1.6.18, and MapChart. RESULTS: The top 100 most cited articles were published between 2014 and 2021, originated from a diverse range of 48 countries, with a predominant focus on the United States of America (USA) and Germany. The top 100 papers were cited between 50 and 712 times. Dreno B, from Nantes University, was the most frequently nominated author. With 12 papers, the Journal of the European Academy of Dermatology and Venereology contributed the most to the top 100 list. Alongside the term "acne", the following terms or phrases were observed frequency in the top 100 articles, Cutibacterium acnes, sebaceous, western diet, antibiotic resistance, staphylococcus-epidermidis, insulinlike growth factor 1, benzoyl peroxide, and polyunsaturated fatty acids. Alongside the term "acne", terms or phrases such as Cutibacterium acnes, sebaceous, western diet, antibiotic resistance, staphylococcus-epidermidis, insulinlike growth factor 1, benzoyl peroxide, and polyunsaturated fatty acids, etc also have a high frequency in the top 100 articles. CONCLUSION: This analysis summarizes the shifting trends of acne research over the last decades. Research on acne is currently flourishing. The related pathogenesis and therapeutic strategies have been the focus of current research and developmental trends in future research.

Knowledge Mapping and Research Hotspots of Generalized Pustular Psoriasis: A Bibliometric Analysis from 2003 to 2023.

Background: Generalised pustular psoriasis (GPP) is a chronic inflammatory skin disease. We aimed to visualize the research hotspots and trends of GPP using bibliometric analysis to enhance our comprehension of the future advancements in both basic science and clinical research. Methods: Relevant publications from July 2003 to July 2023 were obtained from the Web of Science Core Collection on July 12, 2023. The analysis of countries, institutions, authors, references, and keywords associated with this subject was conducted through the utilisation of CiteSpace 6.2.R4, VOSviewer 1.6.18, and Microsoft Excel 2019. Results: A total of 578 papers were analyzed, authored by 2758 researchers from 191 countries/regions and 1868 institutions, published in 174 academic journals. There was an overall upward trajectory in the volume of annual publications, accompanied by a gradual intensification of research interest in GPP. The United States, UDICE-French Research Universities, and Akiyama M of Nagoya University were the most productive and influential country, institution, and author, respectively. The Journal of Dermatology ranked first with the highest publications, and the Journal of the American Academy of Dermatology received the most citations. High-frequency keywords included "generalized pustular psoriasis", "psoriasis, interleukin-36", "plaque psoriasis", "skin-disease", and "antagonist deficiency". Recent research focuses have included "safety", "secukinumab", "spesolimab", "ap1s3 mutations", and "interleukin-36". Burst detection analysis of keywords showed that "moderate", "ixekizumab treatment", "mutations", "efficacy", and "safety" are current research frontiers in this field. Conclusion: This bibliometric analysis delineated the landmark publications in GPP that have defined current research hotspots and development trends, notably the applications, efficacy, and safety of biological agents. Future research endeavors are warranted to explore other biological therapeutic options for both acute GPP and the long-term management of chronic GPP.

Identification of PANoptosis-related biomarkers and immune infiltration characteristics in psoriasis.

BACKGROUND: PANoptosis may play a vital role in psoriasis. We investigated the relationship between PANoptosis in psoriasis. METHODS: Genes information was mainly obtained from GeneCards and the gene expression omnibus database. Genefunctions identification was based on gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses. Gene set enrichment analysis was used to identify enriched signaling pathways in psoriasis. We constructed PPI networks using the search tool for the retrieval of interacting genes database and Cytoscape and explored mRNA-miRNA, mRNA-TF, and mRNA-drug interaction networks. Receiver operating characteristic curves were performed to screen potential biomarkers among these hub genes. Immune cell infiltration was analyzed using the Pearson algorithm, and the correlation between immune-cell abundance and PANoptosis-related differentially expressed gene (PDGs) was investigated. RESULTS: We identified 10 PDGs, which were mainly involved in pyroptosis, cytokine-mediated signaling pathways, Salmonella infection and NOD-like receptor signaling pathway. The activated pathways were mostly proinflammatory and immunoregulatory pathways between immune cells. BAK1, CASP4, IL18, and IRF1 were identified as hub genes in the mRNA-miRNA network, and BAK1, IRF1, and PYCARD were hub genes in the mRNA-TF network. CASP1 was found to be the most targeted gene by drugs or molecular compounds. We found PDGs were positively associated with proinflammatory immune cell infiltration and negatively associated with anti-inflammatory or regulatory immune cells. CONCLUSION: We confirmed the role of PANoptosis in psoriasis for the first time and predicted hub genes and immune characteristics, which provides new ideas for further investigation of psoriasis on pathogenic mechanisms and therapeutic strategies.

Icariin restrains NLRP3 inflammasome-mediated Th2 immune responses and ameliorates atopic dermatitis through modulating a novel lncRNA MALAT1/miR-124-3p axis.

CONTEXT: Atopic dermatitis (AD) is a common inflammatory skin disease characterized with hyperactivation of type 2 T helper (Th2) immune responses. Icariin is a flavonoid glucoside with anti-inflammatory activities, which has been used to treat multiple diseases. OBJECTIVE: The present study investigates the underlying mechanisms by which icariin regulates Th2 responses and AD development. MATERIALS AND METHODS: BALB/c mice were induced by DNFB to establish AD models, and injected with or without 10 mg/kg icariin for 2 weeks (i.p., daily). CD4+T cells were induced by Th2 condition to simulate AD in vitro, and also treated with or without 100 µM icariin. RESULTS: Icariin ameliorated AD-like skin lesion, manifested as a significant decrease in dermatitis scores (from 8.00 ± 1.00 to 3.67 ± 0.58), serum IgE levels (from 3119.15 ± 241.81 to 948.55 ± 182.51 ng/mL), epidermal thickness (from 93.86 ± 4.61 to 42.67 ± 2.48 µm) and infiltration of mast cells (from 60.67 ± 3.21 cells to 36.00 ± 2.65 cells). Also, icariin inactivated NLRP3 inflammasome, inhibited Th2 skewing, reduced lncRNA MALAT1 expression, but elevated miR-124-3p expression in vivo and in vitro. MALAT1 increased NLRP3 expression through targeting miR-124-3p. Knockdown of MALAT1 repressed NLRP3 inflammasome activation and mitigated Th1/Th2 imbalance in Th2-conditioned CD4+T cells, whereas both MALAT1 overexpression and miR-124-3p inhibition ablated the inhibitory effects of icariin on Th2 immune responses. DISCUSSION AND CONCLUSIONS: The findings further improve our understanding of the mechanism by which icariin affects AD progression, and highlights the potential of icariin in the treatment of AD.

Morinda officinalis extract exhibits protective effects against atopic dermatitis by regulating the MALAT1/miR-590-5p/CCR7 axis.

BACKGROUND: Atopic dermatitis (AD) is a chronic inflammatory skin disease with a genetic predisposition, and the traditional Chinese medicine Morinda officinalis and its roots are characterized with anti-inflammatory effects and have been used for the treatment of various disease. However, it is still largely unknown whether Morinda officinalis extract (MOE) can be used for the treatment of AD. OBJECTIVES: In our study we aimed to determine whether MOE could ameliorate 2,4-dinitrochlorobenzene (DNCB)-induced AD and elucidate molecular mechanisms. METHODS: We established an AD mouse model by using DNCB. Skin pathological analysis and ELISA assay were used to detect the effect of MOE on the inflammation of AD model mouse skin and the expression changes of inflammatory factors, and further functional verification was performed in TNF-α/IFN-γ-induced HaCaT cells. RESULTS: Our in vivo experiments confirmed that MOE remarkably reduced DNCB-induced AD lesions and symptoms, such as epidermal and dermal thickness and mast cell infiltration and inflammatory cytokines secretion in the mice models. In addition, the underlying mechanisms by which MOE ameliorated AD had been uncovered, and we verified that MOE inhibited MALAT1 expression in AD, resulting in attenuated expression of C-C chemokine receptor type 7 (CCR7) regulated by MALAT1-sponge miR-590-5p in a competing endogenous RNA (ceRNA) mechanisms-dependent manner, thereby inhibiting TNF-α/IFN-γ-induced cellular proliferation and inflammation.

[Clinical study of modified Yiyi Baijiang Decoction on psoriasis vulgaris due to dampness-heat accumulation].

The present study observed the clinical effect of modified Yiyi Baijiang Decoction on psoriasis vulgaris and explored its influence on growth factors and inflammatory factors in the serum and skin tissues. A total of 130 patients were randomly divided into control group and experimental group, with 65 cases in each group. The patients in the control group received Acitretin Capsules and Calcipotriol Ointment, and those in the experimental group received modified Yiyi Baijiang Decoction combined with external application for four weeks. The psoriasis area and severity index(PASI), blood vessel count in the superficial dermis(SDBVC), skin thickness(STK), and traditional Chinese medicine(TCM) symptoms were observed before and after treatment. The growth factors [epidermal growth factor(EGF), endothelial cell-specific molecule-1(ESM-1), fibroblast growth factor-23(FGF-23), and transforming growth factor-ß1(TGF-ß1)] and inflammatory factors [nuclear factor-κB(NF-κB), prealbumin(PA), CC chemokine ligand 20(CCL20), and procalcitonin(PCT)] in the serum and skin tissues were detected. The total effective rate was 98.5% in the experimental group, higher than that 83.1% in the control group(P<0.05). Compared with the control group after treatment, the experimental group showed decreased PASI, SDBVC, STK, TCM symptoms, ESM-1, FGF-23, TGF-ß1, NF-κB, CCL20, and PCT(P<0.05), and increased EGF and PA(P<0.05). The incidence of adverse events was 1.5% in the experimental group, lower than that 21.5% in the control group(P<0.05). The results showed that modified Yiyi Baijiang Decoction could effectively relieve skin lesions in patients with psoriasis vulgaris and improve the growth factors and inflammatory factors in the serum and skin lesions, with high safety.

Catalpol ameliorates psoriasis-like phenotypes via SIRT1 mediated suppression of NF-κB and MAPKs signaling pathways.

Psoriasis is a chronic inflammatory skin disease that affects approximately 2% of worldwide population, and causing long-term troubles to the patients. Therefore, it is urgent to develop safe and effective therapeutic drugs. Catalpol is a natural iridoid glucoside, that has several remarkable pharmacological effects, however, whether catalpol can alleviated psoriasis has not been explored. The goal of the present work is to study the role of catalpol in psoriasis in vivo and in vitro. Imiquimod-induced psoriasis-like mice were applied with different concentrations of catalpol for 8 consecutive days. The severity degree of psoriasis was estimated and the skin pathological changes were detected by H&E staining. Also, TNF-α-stimulated keratinocytes were treated with different concentrations of catalpol, then the oxidative stress and inflammation factors, as well as the expression of SIRT1 and activation of NF-kB and MAPK pathways were measured. The results showed that catalpol reduced the erythema, scaling, ear thickness, and changed pathological phenotypes in the lesioned skin region in mice. Treatment with catalpol significantly suppressed the oxidative stress and inflammatory reactions in vivo and in vitro, as reflected by the decreased secretion or expression of oxidative stress indicators and proinflammatory factors. Furthermore, the SIRT1 was up-regulated and the NF-κB and MAPKs signaling pathways were suppressed by the treatment of catalpol in vivo and in vitro. In summary, our data suggested that catalpol may have a therapeutic property of psoriasis by ameliorating oxidative stress and inflammation partly through SIRT1 mediated suppression of NF-κB and MAPKs pathways. Abbreviation: CAT: catalase; ELISA: enzyme-linked immunosorbent assay; GSH: glutathione; HRP: horseradish peroxidase; IMQ: imiquimod; JNK: c-Jun NH 2-terminal kinases; MAPKs: mitogen-activated protein kinases; MDA: malondialdehyde; NC: negative control group; NF-kB: nuclear factor kappa B; PASI: psoriasis area and severity index; PVDF: polyvinylidene difluoride membranes; qRT-PCR: quantitative real time polymerase chain reaction; ROS: reactive oxygen species; SDS-PAGE: sodium dodecyl sulfate-polyacrylamide gel; SIRT1: silent information regulator 1; SOD: Cu/Zn superoxide dismutase.

MicroRNA-215-5p inhibits the proliferation of keratinocytes and alleviates psoriasis-like inflammation by negatively regulating DYRK1A and its downstream signalling pathways.

Psoriasis is a chronic inflammatory disease characterized by abnormal hyperproliferation and differentiation. The object of this study is to explore the role of microRNA-215-5p in psoriasis-like inflammation. The expression of miR-215-5p was found to be down-regulated in pro-inflammatory factor-stimulated HaCaT cells and imiquimod (IMQ)-treated skin tissues. Overexpression of miR-215-5p suppressed the proliferation and cell cycle progression of HaCaT cells. Further, miR-215-5p agomir alleviated the disease severity, pathological features and Ki67 positive cells in IMQ-treated mice. Luciferase assay confirmed that miR-215-5p could bind to the 3'UTR of DYRK1A. The in vitro and in vivo results showed that miR-215-5p negatively regulates DYRK1A, which further inhibited EGFR and its downstream signalling pathways, AKT and ERK. Collectively, our results provide evidence that overexpression of miR-215-5p inhibits the proliferation of HaCaT cells and alleviates psoriasis-like inflammation partly by DYRK1A mediated inhibition of the EGFR signalling pathway. miR-215-5p may serve as a novel small molecule for therapeutic intervention in psoriasis.

Cimifugin ameliorates imiquimod-induced psoriasis by inhibiting oxidative stress and inflammation via NF-κB/MAPK pathway.

Cimifugin is an important component of chromones in the dry roots of Saposhikovia divaricata for treating inflammatory diseases. However, the possible effect of cimifugin in psoriasis needs further investigation. This current work was designed to evaluate the effects of cimifugin in psoriasis in vivo and in vitro, and unravel the underlying molecular mechanism. Here, we used imiquimod (IMQ) or tumor necrosis factor (TNF)-α to induce a psoriasis-like model in mice or keratinocytes. Obviously, the results showed that cimifugin reduced epidermal hyperplasia, psoriasis area severity index (PASI) scores, ear thickness and histological psoriasiform lesions in IMQ-induced mice. The decreased levels of reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT), and the accumulation of malondialdehyde (MDA) in skin tissues by IMQ were attenuated by cimifugin. Furthermore, it was observed that cimifugin effectively reversed IMQ-induced up-regulation of proinflammatory cytokines, including TNF-α, IL-6, IL-1ß, IL-17A, and IL-22. Mechanically, we noticed that cimifugin inhibited IMQ-activated phosphorylation of NF-κB (IκB and p65) and MAPK (JNK, ERK, and p38) signaling pathways. Similar alterations for oxidative stress and inflammation parameters were also detected in TNF-α-treated HaCaT cells. In addition, cimifugin-induced down-regulation of ICAM-1 were observed in TNF-α-treated cells. Altogether, our findings suggest that cimifugin protects against oxidative stress and inflammation in psoriasis-like pathogenesis by inactivating NF-κB/MAPK signaling pathway, which may develop a novel and effective drug for the therapy of psoriasis.