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@ARTICLE{ElBounkari:277434,
      author       = {El Bounkari, Omar and Zan, Chunfang and Yang, Bishan and
                      Ebert, Simon and Wagner, Jonas and Bugar, Elina and Kramer,
                      Naomi and Bourilhon, Priscila and Kontos, Christos and
                      Zarwel, Marlies and Sinitski, Dzmitry and Milic, Jelena and
                      Jansen, Yvonne and Kempf, Wolfgang E and Sachs, Nadja and
                      Maegdefessel, Lars and Ji, Hao and Gokce, Ozgun and Riols,
                      Fabien and Haid, Mark and Gerra, Simona and Hoffmann, Adrian
                      and Brandhofer, Markus and Avdic, Maida and Bucala, Richard
                      and Megens, Remco T A and Willemsen, Nienke and Messerer,
                      Denise and Schulz, Christian and Bartelt, Alexander and
                      Harm, Tobias and Rath, Dominik and Döring, Yvonne and
                      Gawaz, Meinrad and Weber, Christian and Kapurniotu,
                      Aphrodite and Bernhagen, Jürgen},
      title        = {{A}n atypical atherogenic chemokine that promotes advanced
                      atherosclerosis and hepatic lipogenesis.},
      journal      = {Nature Communications},
      volume       = {16},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DZNE-2025-00417},
      pages        = {2297},
      year         = {2025},
      abstract     = {Atherosclerosis is the underlying cause of myocardial
                      infarction and ischemic stroke. It is a lipid-triggered and
                      cytokine/chemokine-driven arterial inflammatory condition.
                      We identify D-dopachrome tautomerase/macrophage
                      migration-inhibitory factor-2 (MIF-2), a paralog of the
                      cytokine MIF, as an atypical chemokine promoting both
                      atherosclerosis and hepatic lipid accumulation. In
                      hyperlipidemic Apoe-/- mice, Mif-2-deficiency and
                      pharmacological MIF-2-blockade protect against lesion
                      formation and vascular inflammation in early and advanced
                      atherogenesis. MIF-2 promotes leukocyte migration,
                      endothelial arrest, and foam-cell formation, and we identify
                      CXCR4 as a receptor for MIF-2. Mif-2-deficiency in Apoe-/-
                      mice leads to decreased plasma lipid levels and suppressed
                      hepatic lipid accumulation, characterized by reductions in
                      lipogenesis-related pathways, tri-/diacylglycerides, and
                      cholesterol-esters, as revealed by hepatic
                      transcriptomics/lipidomics. Hepatocyte cultures and
                      FLIM-FRET-microscopy suggest that MIF-2 activates
                      SREBP-driven lipogenic genes, mechanistically involving
                      MIF-2-inducible CD74/CXCR4 complexes and PI3K/AKT but not
                      AMPK signaling. MIF-2 is upregulated in unstable carotid
                      plaques from atherosclerotic patients and its plasma
                      concentration correlates with disease severity in patients
                      with coronary artery disease. These findings establish MIF-2
                      as an atypical chemokine linking vascular inflammation to
                      metabolic dysfunction in atherosclerosis.},
      keywords     = {Animals / Lipogenesis: genetics / Atherosclerosis:
                      metabolism / Atherosclerosis: pathology / Atherosclerosis:
                      genetics / Humans / Mice / Liver: metabolism / Liver:
                      pathology / Intramolecular Oxidoreductases: metabolism /
                      Intramolecular Oxidoreductases: genetics / Male /
                      Chemokines: metabolism / Receptors, CXCR4: metabolism /
                      Receptors, CXCR4: genetics / Mice, Inbred C57BL /
                      Hepatocytes: metabolism / Hepatocytes: pathology /
                      Macrophage Migration-Inhibitory Factors: metabolism /
                      Macrophage Migration-Inhibitory Factors: genetics / Mice,
                      Knockout / Female / Signal Transduction / Foam Cells:
                      metabolism / Intramolecular Oxidoreductases (NLM Chemicals)
                      / Chemokines (NLM Chemicals) / Receptors, CXCR4 (NLM
                      Chemicals) / dopachrome isomerase (NLM Chemicals) /
                      Macrophage Migration-Inhibitory Factors (NLM Chemicals) /
                      CXCR4 protein, mouse (NLM Chemicals)},
      cin          = {AG Gokce},
      ddc          = {500},
      cid          = {I:(DE-2719)1013041},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40055309},
      doi          = {10.1038/s41467-025-57540-z},
      url          = {https://pub.dzne.de/record/277434},
}