{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kim HR"],"funding":["National Research Foundation of Korea(NRF) funded by the Ministry of Science, ICT &amp; Future Planning","National Research Foundation of Korea(NRF) funded by the Ministry of Science, ICT & Future Planning"],"pagination":["3441"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9975446"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(1)"],"pubmed_abstract":["Hyperoxia is frequently used for treating acute respiratory failure, but it can cause acute lung injury. Nucleotide-binding domain and leucine-rich-repeat-containing family member X1 (NLRX1) is localized in mitochondria and involved in production of reactive oxygen species, inflammation, and apoptosis, which are the features of hyperoxic acute lung injury (HALI). The contribution of NLRX1 to HALI has not previously been addressed. Thus, to investigate the role of NLRX1 in hyperoxia, we generated a murine model of HALI in wild-type (WT) and NLRX1<sup>-/-</sup> mice by exposure to > 95% oxygen for 72 h. As a result, NLRX1 expression was elevated in mice exposed to hyperoxia. In acute lung injury, levels of inflammatory cells, protein leakage, cell cytotoxicity, and pro-inflammatory cytokines"],"journal":["Scientific reports"],"pubmed_title":["NLRX1 knockdown attenuates pro-apoptotic signaling and cell death in pulmonary hyperoxic acute injury."],"pmcid":["PMC9975446"],"funding_grant_id":["NRF-2020R1A2B5B02001713","NRF-2022R1F1A1064545"],"pubmed_authors":["Song TW","Sohn MH","Baek SM","Kim EG","Kim MN","Kim KW","Kang MJ","Lee YJ","Leem JS","Kim HR"],"additional_accession":[]},"is_claimable":false,"name":"NLRX1 knockdown attenuates pro-apoptotic signaling and cell death in pulmonary hyperoxic acute injury.","description":"Hyperoxia is frequently used for treating acute respiratory failure, but it can cause acute lung injury. Nucleotide-binding domain and leucine-rich-repeat-containing family member X1 (NLRX1) is localized in mitochondria and involved in production of reactive oxygen species, inflammation, and apoptosis, which are the features of hyperoxic acute lung injury (HALI). The contribution of NLRX1 to HALI has not previously been addressed. Thus, to investigate the role of NLRX1 in hyperoxia, we generated a murine model of HALI in wild-type (WT) and NLRX1<sup>-/-</sup> mice by exposure to > 95% oxygen for 72 h. As a result, NLRX1 expression was elevated in mice exposed to hyperoxia. In acute lung injury, levels of inflammatory cells, protein leakage, cell cytotoxicity, and pro-inflammatory cytokines","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Mar","modification":"2025-04-05T13:02:37.612Z","creation":"2025-04-05T13:02:37.612Z"},"accession":"S-EPMC9975446","cross_references":{"pubmed":["36859435"],"doi":["10.1038/s41598-023-28206-x"]}}