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Fatty acid oxidation in macrophage polarization

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Figure 1: Macrophage FAO is not required for M2 polarization.

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Acknowledgements

Supported by The US National Institutes of Health (Intramural Funds; and NS072241 for M.J.W.), Fondation Leducq (T.F.) and Japan Society for the Promotion of Science (M.N.).

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Authors and Affiliations

  1. Center for Molecular Medicine, National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland, USA

    Mitsunori Nomura, Jie Liu, Ilsa I Rovira & Toren Finkel

  2. Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

    Elsie Gonzalez-Hurtado, Jieun Lee & Michael J Wolfgang

Authors
  1. Mitsunori Nomura
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  2. Jie Liu
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  3. Ilsa I Rovira
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  4. Elsie Gonzalez-Hurtado
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  5. Jieun Lee
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  6. Michael J Wolfgang
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  7. Toren Finkel
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Contributions

M.N. and J.L. performed the experiments; M.N., I.I.R., E.G.-H., J.L., M.J.W. and T.F. analyzed the data; and M.N. and T.F. wrote the manuscript.

Corresponding authors

Correspondence to Michael J Wolfgang or Toren Finkel.

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The authors declare no competing financial interests.

Integrated supplementary information

Supplementary Figure 1 Transport of long-chain fatty acids into the mitochondrial matrix.

Schematic demonstrating the role of CPT1 located on the outer mitochondrial membrane (OMM) and CPT2 on the inner mitochondrial membrane (IMM) in transporting long chain FAs in the form of Acyl-CoA into the mitochondrial matrix. The drug etomoxir is thought to function as a CPT1 inhibitor.

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Nomura, M., Liu, J., Rovira, I. et al. Fatty acid oxidation in macrophage polarization. Nat Immunol 17, 216–217 (2016). https://doi.org/10.1038/ni.3366

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