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Background: The COVID-19 pandemic has caused over 656 million confirmed cases and over 6.6 million deaths worldwide. Chronic kidney disease (CKD) is considered a high-risk factor for COVID-19; therefore, considerable research has been conducted in this field. Therefore, this study aims to conduct a bibliometric analysis of publications related to COVID-19 and CKD. Methods: Publications were retrieved from the Web of Science Core Collection database on 16 January 2023 and screened based on inclusion criteria. Then the authors used Microsoft Excel and CiteSpace to analyze the included publications from the following seven aspects: countries/regions, institutions, journals, authors, cited references, and keywords. Results: In total, 622 publications were included in the study. The USA has the most publications in this field, followed by China. The Icahn School of Medicine at Mount Sinai and Harvard Medical School had the highest number of publications in the field. Journal of Clinical Medicine had the largest number of publications, and Lancet was the most cited journal. Alberto Ortiz was the author with the largest number of publications, but there were no influential authors in this field. The highly cited references are mainly clinical studies on COVID-19. Research hotspots in this field include end-stage recent disease, cardiovascular disease, kidney metastasis, diabetes Mellitus, acute kidney injury, meta-analysis, and consistent plasma. Conclusions: The USA, China, and some European countries and their institutions are major contributors to these publications. End-stage renal disease, acute kidney injury, kidney transplantation and convalescent plasma are current hot topics in the field.
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Objectives: Diabetic nephropathy (DN) is the most common microvascular complication of diabetes mellitus. This study investigated the mechanism of triptolide (TP) in podocyte injury in DN.Methods: DN mouse models were established by feeding with a high-fat diet and injecting with streptozocin and MPC5 podocyte injury models were induced by high-glucose (HG), followed by TP treatment. Fasting blood glucose and renal function indicators, such as 24 h urine albumin (UAlb), serum creatinine (SCr), blood urea nitrogen (BUN), and kidney/body weight ratio of mice were examined. H&E and TUNEL staining were performed for evaluating pathological changes and apoptosis in renal tissue. The podocyte markers, reactive oxygen species (ROS), oxidative stress (OS), serum inflammatory cytokines, nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway-related proteins, and pyroptosis were detected by Western blotting and corresponding kits. MPC5 cell viability and pyroptosis were evaluated by MTT and Hoechst 33342/PI double-fluorescence staining. Nrf2 inhibitor ML385 was used to verify the regulation of TP on Nrf2.Results: TP improved renal function and histopathological injury of DN mice, alleviated podocytes injury, reduced OS and ROS by activating the Nrf2/heme oxygenase-1 (HO-1) pathway, and weakened pyroptosis by inhibiting the nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) inflammasome pathway. In vitro experiments further verified the inhibition of TP on OS and pyroptosis by mediating the Nrf2/HO-1 and NLRP3 inflammasome pathways. Inhibition of Nrf2 reversed the protective effect of TP on MPC5 cells.Conclusions: Overall, TP alleviated podocyte injury in DN by inhibiting OS and pyroptosis via Nrf2/ROS/NLRP3 axis.