A bibliometric analysis of NLRP3 inflammasome in acute lung injury/acute respiratory distress syndrome from 2010 to 2021.

Background: Nod-like receptor family pyrin domain containing 3 (NLRP3) inflammasome is essential in the pathogenesis of acute respiratory distress syndrome (ARDS), a fatal clinical syndrome that deteriorated from acute lung injury (ALI). This bibliometric study aims to offer a thorough insight into the scientific output about NLRP3 inflammasome in ALI/ARDS and explore the intellectual base, developing trajectory and emerging trends. Methods: We retrieved the literature from 2010 to 2021 from Science Citation Index Expanded (SCIE) database. Bibliometrix (3.1.4) R package and CiteSpace (5.8.R3) were used for further analysis and visualization. Results: A total of 508 English articles and reviews published from 2010 to 2021 were identified. The annual number of publications presented a rapidly developing trend especially in recent years. Among all the 42 countries, China was the most productive and most cited country, while the USA had the greatest impact. Peter A. Ward from the USA was the most productive corresponding author, and 4 of these top 10 corresponding authors were from China. The most cited reference was written by Ahmed (2017) of Zhejiang University in China. The Journal of Immunology had highest citation count and G-index. Furthermore, the major disciplines of research front have drifted from "Medicine, Medical, Clinical" to "Molecular, Biology, Immunology" over the past 12 years. In the co-occurring network, the terms "acute lung injury," "NLRP3 inflammasome," "interleukin-1ß," "NF-κB," and "NLRP3 activation" occurred most frequently, while in burst detection, "oxidative stress" had the highest burst strength. Co-citation network revealed that Cluster 2 "virus infection" was the most active area, including the most citation bursts. Cluster 0 "severe COVID-19" and Cluster 1 "dual inhibitor PTUPB" were emerging themes in recent years, and they involved the largest number of publications. Conclusions: This bibliometric analysis revealed a rapid growth trend of the relatively novel topic: NLRP3 inflammasome in ALI/ARDS. China was the largest contributor, while the USA offered the most landmark papers. The major disciplines of research front drifted from "Medicine, Medical, Clinical" to "Molecular, Biology, Immunology." In recent years, studies about the role of NLRP3 in COVID-19-associated ALI/ARDS and oxidative stress became hot spots.

The signaling pathways and therapeutic potential of itaconate to alleviate inflammation and oxidative stress in inflammatory diseases.

Endogenous small molecules are metabolic regulators of cell function. Itaconate is a key molecule that accumulates in cells when the Krebs cycle is disrupted. Itaconate is derived from cis-aconitate decarboxylation by cis-aconitate decarboxylase (ACOD1) in the mitochondrial matrix and is also known as immune-responsive gene 1 (IRG1). Studies have demonstrated that itaconate plays an important role in regulating signal transduction and posttranslational modification through its immunoregulatory activities. Itaconate is also an important bridge among metabolism, inflammation, oxidative stress, and the immune response. This review summarizes the structural characteristics and classical pathways of itaconate, its derivatives, and the compounds that release itaconate. Here, the mechanisms of itaconate action, including its transcriptional regulation of ATF3/IκBζ axis and type I IFN, its protein modification regulation of KEAP1, inflammasome, JAK1/STAT6 pathway, TET2, and TFEB, and succinate dehydrogenase and glycolytic enzyme metabolic action, are presented. Moreover, the roles of itaconate in diseases related to inflammation and oxidative stress induced by autoimmune responses, viruses, sepsis and IRI are discussed in this review. We hope that the information provided in this review will help increase the understanding of cellular immune metabolism and improve the clinical treatment of diseases related to inflammation and oxidative stress.

Bibliometric analysis of global research trends on pyroptosis in lung disease.

Background: Pyroptosis is a lytic pro-inflammatory programmed cell death mode that depends on caspase, inflammasome, and Gasdermin D (GSDMD). A growing number of studies have shown that pyroptosis is closely related to the pathophysiological mechanism of lung. The purpose of this study is to analyze the literature from Science Citation Index Expanded (SCI-expanded) of Web of Science Core Collection (WoSCC) and visualize the current trends and hotspots in the research of pyroptosis in lung disease. Methods: On February 20, 2022, we retrieved all articles on pyroptosis in lung disease from SCI-expanded of WoSCC. Original articles and reviews published in English from 2007 to 2021 were included in the analysis. VOSviewer 1.6.17 and CiteSpace 5.8.R2 were used to analyze the retrieved data and visualize the results. Result: 1798 qualified original articles and reviews on pyroptosis in lung disease were included in the bibliometric analysis. So far, the research in this field is still in a period of growth, and the number of global publications has increased yearly. Among the 66 countries that have published relevant articles, China ranked first in the number of publications, and the USA ranked first in the number of cited articles. Holian,A. was the author with the largest number of articles, including 21 published. The University of California System in the USA was the organization with the largest number of articles, totaling 55. Frontiers in Immunology was the journal with the most publications in pyroptosis. After bibliometric analysis, the frequently used keywords are: "NOD-like receptor3 (NLRP3) inflammasome", "inflammation", "oxidative stress", and "acute lung injury (ALI)". Conclusion: The research on pyroptosis in lung disease is in its growth stage. The information released in this article may help researchers better understand the hotspots and developmental trends in this field, the cooperation network information of authors, countries, and institutions, and the citation correlation between articles. With the in-depth study of the mechanism of pyroptosis, the focus has shifted to increasing research on the connections and influences of different diseases. So far, increasing attention has been paid to the research field of the relationship between ALI and pyroptosis related to COVID-19.

Bibliometric analysis of global research trends on pyroptosis in lung disease

Background Pyroptosis is a lytic pro-inflammatory programmed cell death mode that depends on caspase, inflammasome, and Gasdermin D (GSDMD). A growing number of studies have shown that pyroptosis is closely related to the pathophysiological mechanism of lung. The purpose of this study is to analyze the literature from Science Citation Index Expanded (SCI-expanded) of Web of Science Core Collection (WoSCC) and visualize the current trends and hotspots in the research of pyroptosis in lung disease. Methods On February 20, 2022, we retrieved all articles on pyroptosis in lung disease from SCI-expanded of WoSCC. Original articles and reviews published in English from 2007 to 2021 were included in the analysis. VOSviewer 1.6.17 and CiteSpace 5.8.R2 were used to analyze the retrieved data and visualize the results. Result 1798 qualified original articles and reviews on pyroptosis in lung disease were included in the bibliometric analysis. So far, the research in this field is still in a period of growth, and the number of global publications has increased yearly. Among the 66 countries that have published relevant articles, China ranked first in the number of publications, and the USA ranked first in the number of cited articles. Holian,A. was the author with the largest number of articles, including 21 published. The University of California System in the USA was the organization with the largest number of articles, totaling 55. Frontiers in Immunology was the journal with the most publications in pyroptosis. After bibliometric analysis, the frequently used keywords are: “NOD-like receptor3 (NLRP3) inflammasome”, “inflammation”, “oxidative stress”, and “acute lung injury (ALI)”. Conclusion The research on pyroptosis in lung disease is in its growth stage. The information released in this article may help researchers better understand the hotspots and developmental trends in this field, the cooperation network information of authors, countries, and institutions, and the citation correlation between articles. With the in-depth study of the mechanism of pyroptosis, the focus has shifted to increasing research on the connections and influences of different diseases. So far, increasing attention has been paid to the research field of the relationship between ALI and pyroptosis related to COVID-19.

Magnesium Hydride Ameliorates Endotoxin-Induced Acute Respiratory Distress Syndrome by Inhibiting Inflammation, Oxidative Stress, and Cell Apoptosis

Acute respiratory distress syndrome (ARDS) causes uncontrolled pulmonary inflammation, resulting in high morbidity and mortality in severe cases. Given the antioxidative effect of molecular hydrogen, some recent studies suggest the potential use of molecular hydrogen as a biomedicine for the treatment of ARDS. In this study, we aimed to explore the protective effects of magnesium hydride (MgH2) on two types of ARDS models and its underlying mechanism in a lipopolysaccharide (LPS)-induced ARDS model of the A549 cell line. The results showed that LPS successfully induced oxidative stress, inflammatory reaction, apoptosis, and barrier breakdown in alveolar epithelial cells (AEC). MgH2 can exert an anti-inflammatory effect by down-regulating the expressions of inflammatory cytokines (IL-1β, IL-6, and TNF-α). In addition, MgH2 decreased oxidative stress by eliminating intracellular ROS, inhibited apoptosis by regulating the expressions of cytochrome c, Bax, and Bcl-2, and suppressed barrier breakdown by up-regulating the expression of ZO-1 and occludin. Mechanistically, the expressions of p-AKT, p-mTOR, p-P65, NLRP3, and cleaved-caspase-1 were decreased after MgH2 treatment, indicating that AKT/mTOR and NF-κB/NLRP3/IL-1β pathways participated in the protective effects of MgH2. Furthermore, the in vivo study also demonstrated that MgH2-treated mice had a better survival rate and weaker pathological damage. All these findings demonstrated that MgH2 could exert an ARDS-protective effect by regulating the AKT/mTOR and NF-κB/NLRP3/IL-1β pathways to suppress LPS-induced inflammatory reaction, oxidative stress injury, apoptosis, and barrier breakdown, which may provide a potential strategy for the prevention and treatment of ARDS.

Experience in the diagnosis and treatment of acute biliary tract infection during the epidemic of novel coronavirus pneumonia

On January 20, 2020, WHO defined the epidemic of novel coronavirus pneumonia as a public health emergency of international concern, and the epidemic attracted worldwide attention. While effectively controlling source of infection, cutting off the route of transmission, and protecting the susceptible population, it is of great importance to reduce the delay in the diagnosis and treatment of patients with acute abdominal disease and ensure normal clinical work. Therefore, with reference to the current diagnosis and treatment protocols and guidelines and the actual situation in Boading Second Hospital, this article summarize the experience in outpatient triage, treatment process, operation classification, prevention and control, and ward management for patients with acute biliary tract infection. The analysis process, operation classification, prevention and control, and ward management for patients with acute biliary tract infection. The analysis shows that the formulation of emergency plans for patients with acute biliary tract infection during the epidemic of novel coronavirus pneumonia can help to differentiate such patients from the patients with novel coronavirus pneumonia and avoid transmission and cross-infection of novel coronavirus during standardized diagnosis and treatment of acute biliary tract infection.