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CD36 in Atherosclerosis: Pathophysiological Mechanisms and Therapeutic Implications

Current Atherosclerosis Reports volume 22, Article number: 59 (2020) Cite this article

Abstract

Purpose of Review

Atherosclerosis is a chronic disease characterized by lipid retention and inflammation in the artery wall. The retention and oxidation of low-density lipoprotein (LDL) in sub-endothelial space play a critical role in atherosclerotic plaque formation and destabilization. Oxidized LDL (ox-LDL) and other modified LDL particles are avidly taken up by endothelial cells, smooth muscle cells, and macrophages mainly through several scavenger receptors, including CD36 which is a class B scavenger receptor and membrane glycoprotein.

Recent Findings

Animal studies performed on CD36-deficient mice suggest that deficiency of CD36 prevents the development of atherosclerosis, though with some debate. CD36 serves as a signaling hub protein at the crossroad of inflammation, lipid metabolism, and fatty acid metabolism. In addition, the level of soluble CD36 (unattached to cells) in the circulating blood was elevated in patients with atherosclerosis and other metabolic disorders.

Summary

We performed a state-of-the-art review on the structure, ligands, functions, and regulation of CD36 in the context of atherosclerosis by focusing on the pathological role of CD36 in the dysfunction of endothelial cells, smooth muscle cells, monocytes/macrophages, and platelets. Finally, we highlight therapeutic possibilities to target CD36 expression/activity in atherosclerosis.

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Acknowledgments

The authors were grateful to Prof. Roy Silverstein (Medical College of Wisconsin) for his insightful comments on and proof-reading of this manuscript.

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Author notes

  1. Kunming Tian and Yan Xu contributed equally to this work.

Affiliations

  1. Department of Preventive Medicine, School of Public Health, Zunyi Medical University, Zunyi, Guizhou, China

    Kunming Tian & Yan Xu

  2. Halal Research Center of IRI, FDA, Tehran, Iran

    Amirhossein Sahebkar

  3. Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, 9177948564, Iran

    Amirhossein Sahebkar

  4. Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran

    Amirhossein Sahebkar

  5. Department of Endocrinology and Metabolism, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230037, China

    Suowen Xu

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  1. Kunming Tian
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Tian, K., Xu, Y., Sahebkar, A. et al. CD36 in Atherosclerosis: Pathophysiological Mechanisms and Therapeutic Implications. Curr Atheroscler Rep 22, 59 (2020). https://doi.org/10.1007/s11883-020-00870-8

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Keywords

  • CD36
  • Atherosclerosis
  • Macrophage
  • Endothelial cell
  • Oxidized LDL
  • Lipid metabolism