{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["18(8)"],"submitter":["Zhang H"],"pubmed_abstract":["Neutrophil extracellular traps (NETs) production is a major strategy employed by polymorphonuclear neutrophils (PMNs) to fight against microbes. NETs have been implicated in the pathogenesis of various lung injuries, although few studies have explored NETs in sepsis-associated acute lung injury (SI-ALI). Here, we demonstrate a major contribution of NETs to the pathology of sepsis-associated ALI by inducing ferroptosis of alveolar epithelial cells. Using both <i>in vitro</i> and <i>in vivo</i> studies, our findings show enhanced NETs accumulation in sepsis-associated ALI patients and mice, as well as the closely related upregulation of ferroptosis, the induction of which depends on METTL3-induced m6A modification of GPX4. Using a CLP-induced sepsis-associated ALI mouse model established wit"],"journal":["International journal of biological sciences"],"pagination":["3337-3357"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9134924"],"repository":["biostudies-literature"],"pubmed_title":["Neutrophil extracellular traps mediate m<sup>6</sup>A modification and regulates sepsis-associated acute lung injury by activating ferroptosis in alveolar epithelial cells."],"pmcid":["PMC9134924"],"pubmed_authors":["Liu J","Guo K","Zhang H","Qu M","Miao C","Chen W","Shen R","Zhou Y","Wang Y","Cata JP","Yang S","Sun Z"],"additional_accession":[]},"is_claimable":false,"name":"Neutrophil extracellular traps mediate m<sup>6</sup>A modification and regulates sepsis-associated acute lung injury by activating ferroptosis in alveolar epithelial cells.","description":"Neutrophil extracellular traps (NETs) production is a major strategy employed by polymorphonuclear neutrophils (PMNs) to fight against microbes. NETs have been implicated in the pathogenesis of various lung injuries, although few studies have explored NETs in sepsis-associated acute lung injury (SI-ALI). Here, we demonstrate a major contribution of NETs to the pathology of sepsis-associated ALI by inducing ferroptosis of alveolar epithelial cells. Using both <i>in vitro</i> and <i>in vivo</i> studies, our findings show enhanced NETs accumulation in sepsis-associated ALI patients and mice, as well as the closely related upregulation of ferroptosis, the induction of which depends on METTL3-induced m6A modification of GPX4. Using a CLP-induced sepsis-associated ALI mouse model established wit","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022","modification":"2025-04-05T11:58:26.39Z","creation":"2025-04-05T11:58:26.39Z"},"accession":"S-EPMC9134924","cross_references":{"pubmed":["35637949"],"doi":["10.7150/ijbs.69141"]}}