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Chavakis, T. ; Alexaki, V.I.* ; Ferrante, A.W.*

Macrophage function in adipose tissue homeostasis and metabolic inflammation.

Nat. Immunol. 24, 757-766 (2023)
Verlagsversion DOI PMC
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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter Necrosis-factor-alpha; Insulin-resistance; Myeloid Cells; Tnf-alpha; Local Proliferation; Obesity; Fat; Stress; Infiltration; Myelopoiesis
Sprache englisch
Veröffentlichungsjahr 2023
HGF-Berichtsjahr 2023
ISSN (print) / ISBN 1529-2908
e-ISSN 1529-2916
Zeitschrift Nature Immunology
Quellenangaben Band: 24, Heft: 5, Seiten: 757-766 Artikelnummer: , Supplement: ,
Verlag Nature Publishing Group
Verlagsort Heidelberger Platz 3, Berlin, 14197, Germany
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Pancreatic Islet Research (IPI)
POF Topic(s) 90000 - German Center for Diabetes Research
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-502600-008
Förderungen Boehringer Ingelheim Pharmaceuticals
Saxon State Ministry of Science, Culture and Tourism-SMWK (Sonderzuweisung zur Unterstuetzung profilbestimmender Struktureinheiten der TUD)
Deutsche Forschungsgemeinschaft
European Research Council (LOSYSINCHRON)
DOI 10.1038/s41590-023-01479-0
WOS ID 000962733100002
Scopus ID 85151473348
PubMed ID 37012544
Erfassungsdatum 2023-10-06
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