Current Drug Targets

Francis J. Castellino
Kleiderer-Pezold Professor of Biochemistry
Director, W.M. Keck Center for Transgene Research
Dean Emeritus, College of Science
230 Raclin-Carmichael Hall, University of Notre Dame
Notre Dame, IN 46556


MicroRNAs in Arterial Remodelling, Inflammation and Atherosclerosis

Author(s): C. Weber, A. Schober and A. Zernecke

Affiliation: Rudolf-Virchow-Zentrum/ DFG-Forschungszentrum fur Experimentelle Biomedizin Universitat Wurzburg, Joseph-Schneider Str. 2, Haus D15, 97080 Wurzburg, Germany.

Keywords: microRNAs, remodelling, neointima, smooth muscle cells, atherosclerosis, inflammation, leukocytes, monocytes


Atherosclerosis is now widely appreciated to represent a chronic inflammatory reaction of the vascular wall in response to dyslipidemia and endothelial distress involving the inflammatory recruitment of leukocytes and the activation of resident vascular cells. The proliferative response of smooth muscle cells critically contributes to arterial remodelling. As part of the inflammatory infiltrate, monocytes/macrophages, but also dendritic cells, lymphocytes and neutrophils contribute to the pathogenesis of atherosclerosis. The analysis of microRNA (miR) expression in arterial lesions after balloon injury has revealed fundamental changes in the miR signature comprising many different miRs. Moreover, single miRs have been pinpointed to exert a significant impact on neointimal lesion formation. While studies addressing the profile of miR expression during the development of native atherosclerotic plaques are ongoing, it is conceivable that miRs expressed in inflammatory cell subsets would also affect disease progression. Here we summarize the role of miRs in arterial remodelling and atherosclerosis and putative roles of miRs in vascular inflammation by regulating the differentiation and functions of immune cell subsets. Given the importance of the delicately orchestrated immune response in atherosclerosis and arterial remodelling, miRs will exert profound effects during the evolution of lesion formation and constitute possible targets for therapeutic interventions.

Order Reprints Order Eprints Rights & PermissionsPrintExport

Article Details

Page: [950 - 956]
Pages: 7
DOI: 10.2174/138945010791591377