CD36 as a target for metabolic modulation therapy in cardiac disease

Jan F. C. Glatz*, Fang Wang, Miranda Nabben, Joost J. F. P. Luiken

*Corresponding author for this work

Research output: Contribution to journal(Systematic) Review article peer-review

4 Citations (Web of Science)

Abstract

Introduction: Disturbances in myocardial lipid metabolism are increasingly being recognized as drivers of the development and progression of heart disease. Therefore, there is a need for treatments that can directly target lipid metabolic defects in heart failure. The membrane-associated glycoprotein CD36 plays a pivotal role in governing myocardial lipid metabolism by mediating lipid signaling and facilitating the cellular uptake of long-chain fatty acids. Emerging evidence suggests that CD36 is a prominent target in the treatment of heart failure. Areas covered: This article provides an overview of the key role of CD36 for proper contractile functioning of a healthy heart, its implications in the development of cardiac disease (ischemia/reperfusion, cardiac hypertrophy, and diabetic cardiomyopathy), and its application as a target to normalize cardiac metabolism as part of so-called metabolic modulation therapy. Expert opinion: CD36 appears a promising and effective therapeutic target in the treatment of heart failure. Natural compounds and chemical agents known to alter the amount or subcellular distribution of CD36 or inhibit its functioning, should be evaluated for their potency to correct cardiac metabolism and cure heart disease.

Original languageEnglish
Pages (from-to)393-400
Number of pages8
JournalExpert Opinion on Therapeutic Targets
Volume25
Issue number5
DOIs
Publication statusPublished - 4 May 2021

Keywords

  • Cardiometabolic disease
  • diabetic cardiomyopathy
  • Cd36
  • lipid metabolism
  • subcellular trafficking
  • CD36
  • cardiac disease
  • metabolic modulation therapy
  • FATTY-ACID TRANSLOCASE
  • SUBSTRATE METABOLISM
  • LIPID-ACCUMULATION
  • GENE-EXPRESSION
  • MEMBRANE
  • PROTEIN
  • HEART
  • INHIBITION
  • RECEPTOR
  • BINDING

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