Drug Design, Development and Therapy (Nov 2022)

Biological Mechanisms and Related Natural Inhibitors of CD36 in Nonalcoholic Fatty Liver

  • Feng Y,
  • Sun W,
  • Sun F,
  • Yin G,
  • Liang P,
  • Chen S,
  • Liu X,
  • Jiang T,
  • Zhang F

Journal volume & issue
Vol. Volume 16
pp. 3829 – 3845

Abstract

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Yanan Feng,1,* Wenxiu Sun,2,* Fengcui Sun,1 Guoliang Yin,1 Pengpeng Liang,1 Suwen Chen,1 Xiangyi Liu,1 Tongfei Jiang,3 Fengxia Zhang4 1Shandong University of Traditional Chinese Medicine, Jinan, 250000, People’s Republic of China; 2Department of Nursing, Taishan Vocational College of Nursing, Taian, People’s Republic of China; 3Capital Medical University, Beijing, 100069, People’s Republic of China; 4Department of Neurology, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, 250011, People’s Republic of China*These authors contributed equally to this workCorrespondence: Fengxia Zhang, Department of Neurology, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, 250011, People’s Republic of China, Tel +86-131-5317-5246, Email [email protected]: Non-alcoholic fatty liver disease (NAFLD), a spectrum of liver disorders from non-alcoholic fatty liver (NAFL) to the more severe non-alcoholic steatohepatitis (NASH), is the leading etiology of chronic liver disease and its global prevalence is increasing. Hepatic steatosis, a condition marked by an abnormal buildup of triglycerides in the liver, is the precursor to NAFLD. Differentiated cluster 36 (CD36), a scavenger receptor class B protein, is a membrane receptor that recognizes multiple lipid and non-lipid ligands. It is generally agreed that CD36 contributes significantly to hepatic steatosis by taking part in fatty acid uptake as well as triglyceride storage and secretion. While there has not been any conclusive research on how CD36 inhibitors prevent NAFLD from progressing and no clinically approved CD36 inhibitors are currently available for use in NAFLD, CD36 remains a target worthy of further investigation in NAFLD. In recent years, the potential role of natural products acting through CD36 in treating non-alcoholic fatty liver disease has attracted much attention. This paper offers an overview of the pathogenesis of CD36 in NAFLD and summarizes some of the natural compounds or extracts that are currently being investigated for modulating NAFLD via CD36 or the CD36 pathway, providing an alternative approach to the development of CD36-related drugs in NAFLD.Keywords: NAFLD, CD36, natural inhibitors, FFA, TG

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