{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Abe Y"],"funding":["MEXT | Japan Society for the Promotion of Science (JSPS)","NHLBI NIH HHS","U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI)","American Heart Association (American Heart Association, Inc.)"],"pagination":["1287-1298"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12456008"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["26(8)"],"pubmed_abstract":["Bronchopulmonary dysplasia is a common complication of preterm birth, driven in part by the inflammatory effects of supplemental oxygen on the immature lung. Although oxygen therapy is essential, it contributes to disrupted lung development but not all infants are equally susceptible. Using genetically diverse mouse models, we found that hyperoxia-sensitive mice exhibit a distinct innate immune response compared to resilient strains. Notably, the hyperoxia-sensitive C57BL/6J strain showed selective upregulation of TREM2 on lung macrophages and monocytes. Deletion of TREM2 in myeloid cells led to reduced inflammation, preserved alveolar structure and sustained cell proliferation in the developing lung following oxygen exposure. Mechanistically, TREM2 loss limited p53 activation, favoring ce"],"journal":["Nature immunology"],"pubmed_title":["Genetic variation in the activity of a TREM2-p53 signaling axis determines oxygen-induced lung injury."],"pmcid":["PMC12456008"],"funding_grant_id":["23PRE1025458","R01- HL170183A","201860150","R01 HL170183"],"pubmed_authors":["Longaker MT","Sajti E","Seymour C","Huff R","Ganguly S","Benner C","Dhar D","Guo JL","Glass CK","Jansky S","Lopez DM","Mooney M","Spann NJ","Chanthavixay K","Tang W","Zeng F","Abe Y","Richard JLC"],"additional_accession":[]},"is_claimable":false,"name":"Genetic variation in the activity of a TREM2-p53 signaling axis determines oxygen-induced lung injury.","description":"Bronchopulmonary dysplasia is a common complication of preterm birth, driven in part by the inflammatory effects of supplemental oxygen on the immature lung. Although oxygen therapy is essential, it contributes to disrupted lung development but not all infants are equally susceptible. Using genetically diverse mouse models, we found that hyperoxia-sensitive mice exhibit a distinct innate immune response compared to resilient strains. Notably, the hyperoxia-sensitive C57BL/6J strain showed selective upregulation of TREM2 on lung macrophages and monocytes. Deletion of TREM2 in myeloid cells led to reduced inflammation, preserved alveolar structure and sustained cell proliferation in the developing lung following oxygen exposure. Mechanistically, TREM2 loss limited p53 activation, favoring ce","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Aug","modification":"2026-06-03T18:45:56.536Z","creation":"2026-05-30T03:06:52.558Z"},"accession":"S-EPMC12456008","cross_references":{"pubmed":["40715658"],"doi":["10.1038/s41590-025-02217-4"]}}