Objectives: To review the literature related to bronchopulmonary dysplasia in extremely premature infants, summarize research hotspots, and report trends. Methods: Relevant articles from 2008 to 2020 were retrieved from the Web of Science Core Collection database, and we extracted the following data: title, abstract, year, keywords, author, organization, journal and cited literature. We downloaded the data into CiteSpace (version 5.7.R3) to summarize countries, institutions, journals, and authors. We visualized the data with a knowledge map, collaborative network analysis, cluster analysis, and burst keyword analysis.Results: We identified 610 articles on bronchopulmonary dysplasia in extremely premature infants. The United States had the most articles on this topic (302 articles), followed by Canada (49 articles) and Germany (44 articles). The top three institutions, high-yield journals, and authors were all from the United States. The most common keywords were neurodevelopmental disorders, active perinatal care, mechanical ventilation, inflammation, pulmonary hypertension, low-dose hydrocortisone, development, and patent ductus arteriosus.Conclusions: This study illustrates the trends and frontiers in the study of bronchopulmonary dysplasia in extremely premature infants. The current hot issues are to identify the high-risk factors of bronchopulmonary dysplasia in extremely premature infants, reasonable hormone use, new cell therapy, and management of complications.
Purpose Status epilepticus (SE) is a life-threatening condition causing brain damage, hippocampal necrosis and apoptosis. This study aimed to determine whether microRNA-210 regulates seizure and apoptosis by targeting the TLR4 /NF-κB1 associated signaling pathway. Methods In a pilocarpine-induced epileptic rat model, the expressions of microRNA-210 (miR-210), TLR4, NF-κB1 and caspase-3 were assessed by a quantitative polymerase chain reaction and Western blotting. Tunel detects hippocampal neuron apoptosis. Results We found that miR-210, TLR4, NF-κB1 and caspase-3 were upregulated in the hippocampus of the rat model compared with that of control. The knockdown of miR-210 significantly restored the expression levels of TLR4, NF-κB1 and caspase-3 and increased hippocampal apoptosis. Conclusion These findings showed that the downregulation of miR-210 promoted apoptosis of hippocampal neurons by negatively regulating the TLR4/NF-кB1 signaling pathway.
This study aimed to determine whether microRNA-322-5p regulates seizure and seizure damage by targeting the TLR4/TRAF6/NF-κB-associated inflammatory signaling pathway. In a pilocarpine-induced epileptic rat model, the expressions of miR-322-5p, TLR4, NF-κB, TRAF6, IRF5, IL-1β, and GABA were assessed by a quantitative polymerase chain reaction and western blotting. Tunel detects hippocampal neuron apoptosis. The results showed that the expression of miR-322-5p significantly decreased in status epilepticus (SE) rats. The reduction of miR-322-5p was accompanied by increased levels of pro-inflammatory cytokines, an increased NF-κB expression, and reduced γ-aminobutyric acid (GABA) levels. Exogenous miR-322-5p reduced the expression of inflammatory molecules and increased the GABA levels in SE rats, and also reduced hippocampal neuronal cell apoptosis caused by epilepsy. In conclusion, the miR-322-5p significantly inhibited the TLR4/TRAF6/NF-κB-associated inflammation and reduced neuronal apoptosis, suggesting that its induction may be of potential interest for novel antiseizure medications.
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