{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Martins R"],"funding":["Deutsche Forschungsgemeinschaft (DFG)","European Research Council","MEC | Fundação para a Ciência e a Tecnologia (FCT)","International Postdoctoral Exchange Fellowship Program from the People Republic of China","MOST | National Natural Science Foundation of China (NSFC)","EC | Horizon 2020 Framework Programme (H2020)","European Molecular Biology Organization (EMBO)","'la Caixa' Foundation ('la Caixa')","EC | H2020 | PRIORITY 'Excellent science' | H2020 Marie Skłodowska-Curie Actions (MSCA)","Bundesministerium für Bildung und Forschung (BMBF)"],"pagination":["106-150"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12759084"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["45(1)"],"pubmed_abstract":["Multicellular organisms rely on inter-organ communication networks to maintain vital parameters within a dynamic physiological range. Macrophages are central to this homeostatic control system, sensing and responding to deviations of those parameters to sustain organismal homeostasis. Here, we demonstrate that dysregulation of iron (Fe) metabolism, imposed by the deletion of ferritin H chain (FTH) in mouse parenchymal cells, is sensed by monocyte-derived macrophages. In response, monocyte-derived macrophages support tissue function, energy metabolism, and thermoregulation via a mechanism that sustains the mitochondria of parenchymal cells. Mechanistically, FTH supports a transcriptional program promoting mitochondrial biogenesis in macrophages, involving mitochondrial transcription factor A (TFAM). Moreover, FTH sustains macrophage viability and supports intercellular mitochondrial transfer from donor parenchymal cells. In conclusion, monocyte-derived macrophages cross-regulate iron and energy metabolism to support tissue function and organismal homeostasis."],"journal":["The EMBO journal"],"pubmed_title":["Homeostatic control of energy metabolism by monocyte-derived macrophages."],"pmcid":["PMC12759084"],"funding_grant_id":["20190090","294709-DAMAGECONTROL ERC-2011-AdG","LISBOA-01-0145-FEDER-022170","82030003","grant 01 EO 1502","32171166","H2020-WIDESPREAD-2020-5-952537","MSCA-IF2019-892773","FEDER/29411/2017","UI/BD/152257/2021","PTDC/MED-FSL/4681/2020","HR18-00502","2021.03494.CEECIND","2022.02426.PTDC","ALTF290-2017ARC","EXC 2051; 390713860","REGDAM 707998","MSCA-IF-EF-ST-753236","PTDC/IMI-IMU/5723/2014"],"pubmed_authors":["Pires M","Mallo M","Mesquita M","Ventura P","Wu Q","Novoa A","Figueiredo A","Braza F","Faisca P","Morais VA","Martins R","Soares MP","Wculek SK","Blankehaus B","Cardoso S","Pagnotta S","Jentho E","Sancho D","Singh S","Weis S"],"additional_accession":[]},"is_claimable":false,"name":"Homeostatic control of energy metabolism by monocyte-derived macrophages.","description":"Multicellular organisms rely on inter-organ communication networks to maintain vital parameters within a dynamic physiological range. Macrophages are central to this homeostatic control system, sensing and responding to deviations of those parameters to sustain organismal homeostasis. Here, we demonstrate that dysregulation of iron (Fe) metabolism, imposed by the deletion of ferritin H chain (FTH) in mouse parenchymal cells, is sensed by monocyte-derived macrophages. In response, monocyte-derived macrophages support tissue function, energy metabolism, and thermoregulation via a mechanism that sustains the mitochondria of parenchymal cells. Mechanistically, FTH supports a transcriptional program promoting mitochondrial biogenesis in macrophages, involving mitochondrial transcription factor A (TFAM). Moreover, FTH sustains macrophage viability and supports intercellular mitochondrial transfer from donor parenchymal cells. In conclusion, monocyte-derived macrophages cross-regulate iron and energy metabolism to support tissue function and organismal homeostasis.","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Jan","modification":"2026-06-06T10:37:25.117Z","creation":"2026-05-29T03:11:49.697Z"},"accession":"S-EPMC12759084","cross_references":{"pubmed":["41249508"],"doi":["10.1038/s44318-025-00622-x"]}}