MicroRNA-33 in atherosclerosis etiology and pathophysiology

Atherosclerosis. 2013 Apr;227(2):201-8. doi: 10.1016/j.atherosclerosis.2012.11.025. Epub 2012 Dec 4.

Abstract

MicroRNAs are a group of endogenous, small non-coding RNA molecules that can induce translation repression of target genes within metazoan cells by specific base pairing with the mRNA of target genes. Recently, microRNA-33 has been discovered as a key regulator in the initiation and progression of atherosclerosis. This review highlights the impact of microRNA-33-mediated regulation in the major cardiometabolic risk factors of atherosclerosis including lipid metabolism (HDL biogenesis and cholesterol homeostasis, fatty acid, phospholipid and triglyceride, bile acids metabolism), inflammatory response, insulin signaling and glucose/energy homeostasis, cell cycle progression and proliferation, and myeloid cell differentiation. Understanding the etiology and pathophysiology of microRNA-33 in atherosclerosis may provide basic knowledge for the development of novel therapeutic targets for ameliorating atherosclerosis and cardiovascular disease.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Atherosclerosis / etiology
  • Atherosclerosis / genetics*
  • Atherosclerosis / physiopathology*
  • Bile Acids and Salts / metabolism
  • Cardiovascular System
  • Cell Cycle
  • Cell Differentiation
  • Cell Proliferation
  • Fatty Acids / metabolism
  • Homeostasis
  • Humans
  • Inflammation
  • Insulin / metabolism
  • Lipids
  • MicroRNAs / metabolism*
  • Risk Factors

Substances

  • Bile Acids and Salts
  • Fatty Acids
  • Insulin
  • Lipids
  • MIRN33a microRNA, human
  • MicroRNAs