Kupffer cell programming by maternal obesity triggers fatty liver disease.

ABSTRACT: Kupffer 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 functions^1-3. 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 expose

SUBMITTER: Huang H 

PROVIDER: S-EPMC12367551 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature