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ATVB Named Lecture Review

2016 ATVB Plenary Lecture

Receptor for Advanced Glycation Endproducts and Implications for the Pathogenesis and Treatment of Cardiometabolic Disorders: Spotlight on the Macrophage

Ann Marie Schmidt
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https://doi.org/10.1161/ATVBAHA.117.307263
Arteriosclerosis, Thrombosis, and Vascular Biology. 2017;37:613-621
Originally published February 9, 2017
Ann Marie Schmidt
From the Diabetes Research Program, Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, New York University School of Medicine, New York.
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This article has a correction. Please see:

  • Correction to: 2016 ATVB Plenary Lecture: Receptor for Advanced Glycation Endproducts and Implications for the Pathogenesis and Treatment of Cardiometabolic Disorders: Spotlight on the Macrophage - June 01, 2017
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    • Receptor for Advanced Glycation Endproducts: A Multiligand Receptor of the Immunoglobulin Superfamily
    • RAGE and Atherosclerosis
    • RAGE and High-Fat Diet–Induced Obesity
    • RAGE and Signal Transduction
    • Acknowledgments
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    Figure.

    Receptor for advanced glycation endproducts (RAGE) and monocyte/macrophage perturbation. The unique cadre of RAGE ligands, via RAGE, stimulates key perturbations in monocytes/macrophages, such as induction of oxidative stress and consequent activation of nuclear factor (NF)-κB; migration (at least in response to RAGE ligand-mediated upregulation of adhesion molecules and chemokines on endothelial cells); downregulation of cholesterol transporters ABCG1 (ATP-binding cassette sub-family G member 1) and ABCA1 (ATP-binding cassette sub-family A member 1), leading to suppression of cholesterol efflux; and downregulation of PPARG and other mediators that tip the balance to increased expression of proinflammatory vs reduced expression of anti-inflammatory mediators, thereby contributing to sustained inflammation and tissue damage. These facets of RAGE pathobiology in macrophages have implications for atherosclerosis and diet-induced obesity, as well as for chronic inflammatory disorders. More study needs to be done to determine whether RAGE modulates glucose/fatty acid metabolism in these cells and whether such effects might affect macrophage properties in responses to stress. Findings to date suggest that targeting RAGE may be beneficial in chronic immunometabolic disorders and that biomarking RAGE activity in circulating monocytes/monocyte-derived macrophages may be a key strategy to track target engagement for future clinical trials. HDL indicates high-density lipoprotein; ICAM1, intercellular adhesion molecule 1; MCP1, monocyte chemotactic protein 1; PPARγ, peroxisome proliferator-activated receptor gamma; ROS, reactive oxygen species; and VCAM1, vascular cell adhesion molecule 1.

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Arteriosclerosis, Thrombosis, and Vascular Biology
April 2017, Volume 37, Issue 4
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    • Receptor for Advanced Glycation Endproducts: A Multiligand Receptor of the Immunoglobulin Superfamily
    • RAGE and Atherosclerosis
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    • RAGE and Signal Transduction
    • Acknowledgments
    • Sources of Funding
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    2016 ATVB Plenary Lecture
    Ann Marie Schmidt
    Arteriosclerosis, Thrombosis, and Vascular Biology. 2017;37:613-621, originally published February 9, 2017
    https://doi.org/10.1161/ATVBAHA.117.307263

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    2016 ATVB Plenary Lecture
    Ann Marie Schmidt
    Arteriosclerosis, Thrombosis, and Vascular Biology. 2017;37:613-621, originally published February 9, 2017
    https://doi.org/10.1161/ATVBAHA.117.307263
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