{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Xian H"],"funding":["University of California San Diego","NCRR NIH HHS","NIA NIH HHS","NIAID NIH HHS","NIEHS NIH HHS","NCI NIH HHS","NINDS NIH HHS","NIAMS NIH HHS","NIH HHS"],"pagination":["1463-1477.e11"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8189765"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["54(7)"],"pubmed_abstract":["Acute respiratory distress syndrome (ARDS), an inflammatory condition with high mortality rates, is common in severe COVID-19, whose risk is reduced by metformin rather than other anti-diabetic medications. Detecting of inflammasome assembly in post-mortem COVID-19 lungs, we asked whether and how metformin inhibits inflammasome activation while exerting its anti-inflammatory effect. We show that metformin inhibited NLRP3 inflammasome activation and interleukin (IL)-1β production in cultured and alveolar macrophages along with inflammasome-independent IL-6 secretion, thus attenuating lipopolysaccharide (LPS)- and SARS-CoV-2-induced ARDS. By targeting electron transport chain complex 1 and independently of AMP-activated protein kinase (AMPK) or NF-κB, metformin blocked LPS-induced and ATP-de"],"journal":["Immunity"],"pubmed_title":["Metformin inhibition of mitochondrial ATP and DNA synthesis abrogates NLRP3 inflammasome activation and pulmonary inflammation."],"pmcid":["PMC8189765"],"funding_grant_id":["P30 AR073761","R01 NS095894","RF1 AG057409","K01 AR077111","U54 CA260591","K26 OD010945","R01 AI072726","P30 CA023100","P42 ES010337","K26 RR026099","R01 AI043477"],"pubmed_authors":["Rundberg Nilsson A","de la Torre JC","Aleman-Muench GR","Tourtellotte WG","Kang S","Trudler D","Lipton SA","Luevanos M","Sanchez-Lopez E","Arditi M","Soroosh P","Liu Y","Teijaro J","Zhang Y","Chen W","Xian H","Gatchalian R","Lewis G","Crother TR","Karin M"],"additional_accession":[]},"is_claimable":false,"name":"Metformin inhibition of mitochondrial ATP and DNA synthesis abrogates NLRP3 inflammasome activation and pulmonary inflammation.","description":"Acute respiratory distress syndrome (ARDS), an inflammatory condition with high mortality rates, is common in severe COVID-19, whose risk is reduced by metformin rather than other anti-diabetic medications. Detecting of inflammasome assembly in post-mortem COVID-19 lungs, we asked whether and how metformin inhibits inflammasome activation while exerting its anti-inflammatory effect. We show that metformin inhibited NLRP3 inflammasome activation and interleukin (IL)-1β production in cultured and alveolar macrophages along with inflammasome-independent IL-6 secretion, thus attenuating lipopolysaccharide (LPS)- and SARS-CoV-2-induced ARDS. By targeting electron transport chain complex 1 and independently of AMP-activated protein kinase (AMPK) or NF-κB, metformin blocked LPS-induced and ATP-de","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Jul","modification":"2026-05-09T05:05:51.631Z","creation":"2022-02-11T16:07:23.201Z"},"accession":"S-EPMC8189765","cross_references":{"pubmed":["34115964"],"doi":["10.1016/j.immuni.2021.05.004"]}}