{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Caratti G"],"funding":["Deutscher Akademischer Austauschdienst","Centre National de la Recherche Scientifique","Institut National de la Santé et de la Recherche Médicale","Fondation pour la Recherche Médicale"],"pagination":["e55363"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9900347"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["24(2)"],"pubmed_abstract":["Macrophages are key cells after tissue damage since they mediate both acute inflammatory phase and regenerative inflammation by shifting from pro-inflammatory to restorative cells. Glucocorticoids (GCs) are the most potent anti-inflammatory hormone in clinical use, still their actions on macrophages are not fully understood. We show that the metabolic sensor AMP-activated protein kinase (AMPK) is required for GCs to induce restorative macrophages. GC Dexamethasone activates AMPK in macrophages and GC receptor (GR) phosphorylation is decreased in AMPK-deficient macrophages. Loss of AMPK in macrophages abrogates the GC-induced acquisition of their repair phenotype and impairs GC-induced resolution of inflammation in vivo during post-injury muscle regeneration and acute lung injury. Mechanist"],"journal":["EMBO reports"],"pubmed_title":["Macrophagic AMPKα1 orchestrates regenerative inflammation induced by glucocorticoids."],"pmcid":["PMC9900347"],"funding_grant_id":["DEQ20140329495"],"pubmed_authors":["Mounier R","Koenen M","Caratti G","Stifel U","Fessard A","Theret M","Desgeorges T","Skurk C","Chazaud B","Tuckermann JP","Juban G","Caratti B"],"additional_accession":[]},"is_claimable":false,"name":"Macrophagic AMPKα1 orchestrates regenerative inflammation induced by glucocorticoids.","description":"Macrophages are key cells after tissue damage since they mediate both acute inflammatory phase and regenerative inflammation by shifting from pro-inflammatory to restorative cells. Glucocorticoids (GCs) are the most potent anti-inflammatory hormone in clinical use, still their actions on macrophages are not fully understood. We show that the metabolic sensor AMP-activated protein kinase (AMPK) is required for GCs to induce restorative macrophages. GC Dexamethasone activates AMPK in macrophages and GC receptor (GR) phosphorylation is decreased in AMPK-deficient macrophages. Loss of AMPK in macrophages abrogates the GC-induced acquisition of their repair phenotype and impairs GC-induced resolution of inflammation in vivo during post-injury muscle regeneration and acute lung injury. Mechanist","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Feb","modification":"2025-05-29T22:09:08.519Z","creation":"2024-11-09T08:44:19.007Z"},"accession":"S-EPMC9900347","cross_references":{"pubmed":["36520372"],"doi":["10.15252/embr.202255363"]}}