Macrophage function in adipose tissue homeostasis and metabolic inflammation.
Autor: | Chavakis T; Institute for Clinical Chemistry and Laboratory Medicine, University Hospital and Faculty of Medicine, Technische Universität Dresden, Dresden, Germany. triantafyllos.chavakis@uniklinikum-dresden.de.; Paul Langerhans Institute Dresden of the Helmholtz Center Munich, University Hospital and Faculty of Medicine, Technische Universität Dresden, Dresden, Germany. triantafyllos.chavakis@uniklinikum-dresden.de.; German Center for Diabetes Research (DZD), Neuherberg, Germany. triantafyllos.chavakis@uniklinikum-dresden.de.; Centre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK. triantafyllos.chavakis@uniklinikum-dresden.de., Alexaki VI; Institute for Clinical Chemistry and Laboratory Medicine, University Hospital and Faculty of Medicine, Technische Universität Dresden, Dresden, Germany., Ferrante AW Jr; Department of Medicine, Institute of Human Nutrition, Naomi Berrie Diabetes Center, Columbia University, New York, NY, USA. |
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Jazyk: | angličtina |
Zdroj: | Nature immunology [Nat Immunol] 2023 May; Vol. 24 (5), pp. 757-766. Date of Electronic Publication: 2023 Apr 03. |
DOI: | 10.1038/s41590-023-01479-0 |
Abstrakt: | Obesity-related metabolic organ inflammation contributes to cardiometabolic disorders. In obese individuals, changes in lipid fluxes and storage elicit immune responses in the adipose tissue (AT), including expansion of immune cell populations and qualitative changes in the function of these cells. Although traditional models of metabolic inflammation posit that these immune responses disturb metabolic organ function, studies now suggest that immune cells, especially AT macrophages (ATMs), also have important adaptive functions in lipid homeostasis in states in which the metabolic function of adipocytes is taxed. Adverse consequences of AT metabolic inflammation might result from failure to maintain local lipid homeostasis and long-term effects on immune cells beyond the AT. Here we review the complex function of ATMs in AT homeostasis and metabolic inflammation. Additionally, we hypothesize that trained immunity, which involves long-term functional adaptations of myeloid cells and their bone marrow progenitors, can provide a model by which metabolic perturbations trigger chronic systemic inflammation. (© 2023. Springer Nature America, Inc.) |
Databáze: | MEDLINE |
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