MicroRNA-126,-145, and -155 A Therapeutic Triad in Atherosclerosis?

Yuanyuan Wei, Maliheh Nazari-Jahantigh, Peter Neth, Christian Weber, Andreas Schober*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

164 Citations (Web of Science)

Abstract

Atherosclerosis is a condition caused by lipid-induced inflammation of the vessel wall orchestrated by a complex interplay of various cell types, such as endothelial cells, smooth muscle cells, and macrophages. MicroRNAs (miRNAs) have emerged as key regulators of gene expression typically by repressing the target mRNA, which determines cell fate and function under homeostatic and disease conditions. Here, we outline the effects of miRNA-145, -126, and -155 in atherosclerosis in vivo. Downregulation of miR-145, which controls differentiation of smooth muscle cells, promotes lesion formation, whereas the endothelial cell-specific miRNA-126 signals the need for endothelial repair through its transfer from apoptotic endothelial cells in microvesicles. Elevated miR-155 levels are characteristic of proinflammatory macrophages and atherosclerotic lesions. However, the effects of miR-155 seem to be different in early and advanced atherosclerosis. The discovery of the role of these miRNAs in atherosclerosis sheds light on the current concepts of atherogenesis and may provide novel treatment options for cardiovascular diseases. (Arterioscler Thromb Vasc Biol. 2013;33:449-454.)
Original languageEnglish
Pages (from-to)449-454
JournalArteriosclerosis Thrombosis and Vascular Biology
Volume33
Issue number3
DOIs
Publication statusPublished - Mar 2013

Keywords

  • endothelial cells
  • Kruppel factor
  • microRNAs
  • smooth muscle cells

Cite this