{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ma L"],"funding":["Ministry of Science and Technology of the People’s Republic of China","Strategic Priority Research Program of the Chinese Academy of Sciences","National Natural Science Foundation of China"],"pagination":["1385-1400"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9225223"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["18(6)"],"pubmed_abstract":["Macrophages rapidly undergo glycolytic reprogramming in response to macroautophagy/autophagy, inflammasome activation and pyroptosis for the clearance of bacteria. Identification the key molecules involved in these three events will provide critical potential therapeutic applications. Upon <i>S. typhimurium</i> infection, FLT4/VEGFR3 and its ligand VEGFC were inducibly expressed in macrophages, and FLT4 signaling inhibited CASP1 (caspase 1)-dependent inflammasome activation and pyroptosis but enhanced MAP1LC3/LC3 activation for elimination of the bacteria. Consistently, FLT4 mutants lacking the extracellular ligand-binding domain increased production of the proinflammatory metabolites such as succinate and lactate, and reduced antimicrobial metabolites including citrate and NAD(P)H in macr"],"journal":["Autophagy"],"pubmed_title":["FLT4/VEGFR3 activates AMPK to coordinate glycometabolic reprogramming with autophagy and inflammasome activation for bacterial elimination."],"pmcid":["PMC9225223"],"funding_grant_id":["2016YFC0905902","2016YFC0905900","2016YFD0500407","81930038","2016YFD0500207","2018YFA0800702","30671038","81630043","81801575","81671572","81701569","31700781","81825011","XDB19000000","81961160738","81571552"],"pubmed_authors":["Qi L","Ma L","Wei B","Lu Y","Zhang L","Wang H","Yu H","Li N","Li W","He Y","Zhang Y","Zhao Q","Zhou F","Wu Y"],"additional_accession":[]},"is_claimable":false,"name":"FLT4/VEGFR3 activates AMPK to coordinate glycometabolic reprogramming with autophagy and inflammasome activation for bacterial elimination.","description":"Macrophages rapidly undergo glycolytic reprogramming in response to macroautophagy/autophagy, inflammasome activation and pyroptosis for the clearance of bacteria. Identification the key molecules involved in these three events will provide critical potential therapeutic applications. Upon <i>S. typhimurium</i> infection, FLT4/VEGFR3 and its ligand VEGFC were inducibly expressed in macrophages, and FLT4 signaling inhibited CASP1 (caspase 1)-dependent inflammasome activation and pyroptosis but enhanced MAP1LC3/LC3 activation for elimination of the bacteria. Consistently, FLT4 mutants lacking the extracellular ligand-binding domain increased production of the proinflammatory metabolites such as succinate and lactate, and reduced antimicrobial metabolites including citrate and NAD(P)H in macr","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jun","modification":"2025-04-22T08:00:26.201Z","creation":"2025-04-05T22:20:43.037Z"},"accession":"S-EPMC9225223","cross_references":{"pubmed":["34632918"],"doi":["10.1080/15548627.2021.1985338"]}}