1. Academic Validation
  2. Pathophysiology of human genetic CD36 deficiency

Pathophysiology of human genetic CD36 deficiency

  • Trends Cardiovasc Med. 2003 May;13(4):136-41. doi: 10.1016/s1050-1738(03)00026-4.
Ken-ichi Hirano 1 Takahiro Kuwasako Yumiko Nakagawa-Toyama Mohamed Janabi Shizuya Yamashita Yuji Matsuzawa
Affiliations

Affiliation

  • 1 Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Suita, Japan. khirano@kb3.so-net.ne.jp
Abstract

CD36, originally identified as glycoprotein IV on platelets, is an 88-kDa integral membrane protein that has multiple ligands and is expressed in the cardiovascular system (ie, blood vessel walls and the heart). Human genetic CD36 deficiency is relatively frequent in Asian and African populations. Investigation into the pathophysiology of this disorder has shown that CD36 may play an important role as a major scavenger receptor for oxidized low-density lipoproteins and as a crucial transporter for long-chain fatty acids. The CD36 deficiency may be related to the phenotypic expression of the "metabolic syndrome," which is frequently associated with atherosclerotic cardiovascular diseases. It also has been reported that CD36 deficiency might be linked with cardiomyopathy. These data raised the possibility that CD36 deficiency might be an important genetic background for these life-threatening human cardiovascular diseases.

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