The role of Kupffer cells in hepatic iron and lipid metabolism
Author(s): ,
Martin Guilliams
Affiliations:
Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium
Corresponding authors. Addresses: Laboratory of Myeloid Cell Ontogeny and Functional Specialization, VIB-UGent Center for Inflammation Research, Technologiepark 927, Ghent, Belgium.
Charlotte L. Scott
Affiliations:
Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK
Corresponding authors. Addresses: Laboratory of Myeloid Cell Ontogeny and Functional Specialization, VIB-UGent Center for Inflammation Research, Technologiepark 927, Ghent, Belgium.
EASL LiverTree™. Guilliams M. Nov 1, 2018; 256717
Martin Guilliams
Martin Guilliams

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[1]. Y. Okabe - Tissue biology perspective on macrophages
[2]. C.L. Scott - Bone marrow-derived monocytes give rise to self-renewing and fully differentiated Kupffer cells
[3]. M. Nairz - “Pumping iron-”how macrophages handle iron at the systemic, microenvironmental, and cellular levels
[4]. I. Theurl - On-demand erythrocyte disposal and iron recycling requires transient macrophages in the liver
[5]. A. Remmerie - Macrophages and lipid metabolism
[6]. A. Leroux - Toxic lipids stored by Kupffer cells correlates with their pro-inflammatory phenotype at an early stage of steatohepatitis
[7]. O. Krenkel - Liver macrophages in tissue homeostasis and disease
[8]. W. Luo - Effect of modulation of PPAR-γ activity on Kupffer cells M1/M2 polarization in the development of non-alcoholic fatty liver disease
[9]. Y.-H. Han - RORα induces KLF4-mediated M2 polarization in the liver macrophages that protect against nonalcoholic steatohepatitis
[10]. K.M. Hart - Type 2 immunity is protective in metabolic disease but exacerbates NAFLD collaboratively with TGF-β
[11]. M. Nahrendorf - Abandoning M1/M2 for a network model of macrophage function
[12]. L. Devisscher - Non-alcoholic steatohepatitis induces transient changes within the liver macrophage pool
[13]. O. Krenkel - Therapeutic inhibition of inflammatory monocyte recruitment reduces steatohepatitis and liver fibrosis
[14]. E. Aigner - Dysregulation of iron and copper homeostasis in nonalcoholic fatty liver
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