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000280788 037__ $$aDZNE-2025-00972
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000280788 1001_ $$0P:(DE-HGF)0$$aHuang, Hao$$b0
000280788 245__ $$aKupffer cell programming by maternal obesity triggers fatty liver disease.
000280788 260__ $$aLondon [u.a.]$$bNature Publ. Group$$c2025
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000280788 520__ $$aKupffer cells (KCs) are tissue-resident macrophages that colonize the liver early during embryogenesis1. Upon liver colonization, KCs rapidly acquire a tissue-specific transcriptional signature, mature alongside the developing liver and adapt to its functions1-3. Throughout development and adulthood, KCs perform distinct core functions that are essential for liver and organismal homeostasis, including supporting fetal erythropoiesis, postnatal erythrocyte recycling and liver metabolism4. However, whether perturbations of macrophage core functions during development contribute to or cause disease at postnatal stages is poorly understood. Here, we utilize a mouse model of maternal obesity to perturb KC functions during gestation. We show that offspring exposed to maternal obesity develop fatty liver disease, driven by aberrant developmental programming of KCs that persists into adulthood. Programmed KCs promote lipid uptake by hepatocytes through apolipoprotein secretion. KC depletion in neonate mice born to obese mothers, followed by replenishment with naive monocytes, rescues fatty liver disease. Furthermore, genetic ablation of the gene encoding hypoxia-inducible factor-α (HIF1α) in macrophages during gestation prevents the metabolic programming of KCs from oxidative phosphorylation to glycolysis, thereby averting the development of fatty liver disease. These results establish developmental perturbation of KC functions as a causal factor in fatty liver disease in adulthood and position fetal-derived macrophages as critical intergenerational messengers within the concept of developmental origins of health and diseases5.
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000280788 650_7 $$2NLM Chemicals$$aHypoxia-Inducible Factor 1, alpha Subunit
000280788 650_7 $$2NLM Chemicals$$aHif1a protein, mouse
000280788 650_2 $$2MeSH$$aAnimals
000280788 650_2 $$2MeSH$$aKupffer Cells: metabolism
000280788 650_2 $$2MeSH$$aKupffer Cells: pathology
000280788 650_2 $$2MeSH$$aKupffer Cells: cytology
000280788 650_2 $$2MeSH$$aFemale
000280788 650_2 $$2MeSH$$aMice
000280788 650_2 $$2MeSH$$aPregnancy
000280788 650_2 $$2MeSH$$aHypoxia-Inducible Factor 1, alpha Subunit: genetics
000280788 650_2 $$2MeSH$$aHypoxia-Inducible Factor 1, alpha Subunit: metabolism
000280788 650_2 $$2MeSH$$aHypoxia-Inducible Factor 1, alpha Subunit: deficiency
000280788 650_2 $$2MeSH$$aPregnancy in Obesity: pathology
000280788 650_2 $$2MeSH$$aPregnancy in Obesity: metabolism
000280788 650_2 $$2MeSH$$aFatty Liver: pathology
000280788 650_2 $$2MeSH$$aFatty Liver: etiology
000280788 650_2 $$2MeSH$$aFatty Liver: metabolism
000280788 650_2 $$2MeSH$$aMale
000280788 650_2 $$2MeSH$$aLiver: metabolism
000280788 650_2 $$2MeSH$$aLiver: pathology
000280788 650_2 $$2MeSH$$aLiver: embryology
000280788 650_2 $$2MeSH$$aLiver: cytology
000280788 650_2 $$2MeSH$$aGlycolysis
000280788 650_2 $$2MeSH$$aHepatocytes: metabolism
000280788 650_2 $$2MeSH$$aAnimals, Newborn
000280788 650_2 $$2MeSH$$aDisease Models, Animal
000280788 650_2 $$2MeSH$$aOxidative Phosphorylation
000280788 650_2 $$2MeSH$$aPrenatal Exposure Delayed Effects: pathology
000280788 650_2 $$2MeSH$$aMice, Inbred C57BL
000280788 650_2 $$2MeSH$$aMacrophages: metabolism
000280788 650_2 $$2MeSH$$aObesity: complications
000280788 693__ $$0EXP:(DE-2719)PRECISE-20190321$$5EXP:(DE-2719)PRECISE-20190321$$ePlatform for Single Cell Genomics and Epigenomics at DZNE  University of Bonn$$x0
000280788 7001_ $$0P:(DE-2719)9002224$$aBalzer, Nora$$b1$$udzne
000280788 7001_ $$00000-0002-0399-1896$$aSeep, Lea$$b2
000280788 7001_ $$aSplichalova, Iva$$b3
000280788 7001_ $$aBlank-Stein, Nelli$$b4
000280788 7001_ $$00000-0003-0660-9506$$aViola, Maria Francesca$$b5
000280788 7001_ $$00009-0009-2227-6765$$aFranco Taveras, Eliana$$b6
000280788 7001_ $$00009-0002-7838-9928$$aAcil, Kerim$$b7
000280788 7001_ $$00009-0008-1572-4390$$aFink, Diana$$b8
000280788 7001_ $$aPetrovic, Franzisca$$b9
000280788 7001_ $$0P:(DE-2719)9002664$$aMakdissi, Nikola$$b10$$udzne
000280788 7001_ $$00000-0001-7077-8748$$aBayar, Seyhmus$$b11
000280788 7001_ $$00009-0007-4879-032X$$aMauel, Katharina$$b12
000280788 7001_ $$00009-0007-7908-1067$$aRadwaniak, Carolin$$b13
000280788 7001_ $$00000-0002-5932-4849$$aZurkovic, Jelena$$b14
000280788 7001_ $$00000-0003-1315-8336$$aKayvanjoo, Amir H$$b15
000280788 7001_ $$00000-0003-1237-7510$$aWunderling, Klaus$$b16
000280788 7001_ $$00009-0007-5929-0064$$aJessen, Malin$$b17
000280788 7001_ $$aYaghmour, Mohamed H$$b18
000280788 7001_ $$00000-0003-2184-1338$$aKenner, Lukas$$b19
000280788 7001_ $$0P:(DE-2719)9000845$$aUlas, Thomas$$b20
000280788 7001_ $$00000-0001-9524-6633$$aGrein, Stephan$$b21
000280788 7001_ $$0P:(DE-2719)2811660$$aSchultze, Joachim L$$b22$$udzne
000280788 7001_ $$00000-0003-4914-6580$$aScott, Charlotte L$$b23
000280788 7001_ $$aGuilliams, Martin$$b24
000280788 7001_ $$00000-0002-3117-0833$$aLiu, Zhaoyuan$$b25
000280788 7001_ $$00000-0002-2857-7755$$aGinhoux, Florent$$b26
000280788 7001_ $$0P:(DE-2719)2812219$$aBeyer, Marc D$$b27
000280788 7001_ $$00000-0001-5161-2558$$aThiele, Christoph$$b28
000280788 7001_ $$00000-0003-1000-7989$$aMeissner, Felix$$b29
000280788 7001_ $$aHasenauer, Jan$$b30
000280788 7001_ $$0P:(DE-2719)9002895$$aWachten, Dagmar$$b31
000280788 7001_ $$00000-0003-2318-2356$$aMass, Elvira$$b32
000280788 773__ $$0PERI:(DE-600)1413423-8$$a10.1038/s41586-025-09190-w$$gVol. 644, no. 8077, p. 790 - 798$$n8077$$p790 - 798$$tNature$$v644$$x0028-0836$$y2025
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