About this item:

383 Views | 435 Downloads

Author Notes:

Correspondence to: hanjoong.jo@bme.gatech.edu

Conflict of interest: The authors have declared no conflicts of interest for this article.

Subject:

Research Funding:

This work was supported by funding from National Institutes of Health grants HL119798, HL113451, HL095070, and HL124879 to HJ.

HJ is John and Jan Portman Professor.

RS is an American Heart Association predoctoral fellow and ST is supported by a postdoc fellowship from the American Heart Association.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Medicine, Research & Experimental
  • Research & Experimental Medicine
  • NITRIC-OXIDE SYNTHASE
  • WALL SHEAR-STRESS
  • ACTIVATED PROTEIN-KINASE
  • NF-KAPPA-B
  • E-DEFICIENT MICE
  • CORONARY-ARTERY-DISEASE
  • DIFFERENTIAL DNA METHYLATION
  • FLOW-DEPENDENT REGULATION
  • PARTIAL CAROTID LIGATION
  • LACKING APOLIPOPROTEIN-E

Omics-based approaches to understand mechanosensitive endothelial biology and atherosclerosis

Tools:

Journal Title:

Wiley Interdisciplinary Reviews: Systems Biology and Medicine

Volume:

Volume 8, Number 5

Publisher:

, Pages 378-401

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Atherosclerosis is a multifactorial disease that preferentially occurs in arterial regions exposed to d-flow can be used to indicate disturbed flow or disturbed blood flow. The mechanisms by which d-flow induces atherosclerosis involve changes in the transcriptome, methylome, proteome, and metabolome of multiple vascular cells, especially endothelial cells. Initially, we begin with the pathogenesis of atherosclerosis and the changes that occur at multiple levels owing to d-flow, especially in the endothelium. Also, there are a variety of strategies used for the global profiling of the genome, transcriptome, miRNA-ome, DNA methylome, and metabolome that are important to define the biological and pathophysiological mechanisms of endothelial dysfunction and atherosclerosis. Finally, systems biology can be used to integrate these ‘omics’ datasets, especially those that derive data based on a single animal model, in order to better understand the pathophysiology of atherosclerosis development in a holistic manner and how this integrative approach could be used to identify novel molecular diagnostics and therapeutic targets to prevent or treat atherosclerosis. WIREs Syst Biol Med 2016, 8:378–401. doi: 10.1002/wsbm.1344. For further resources related to this article, please visit the WIREs website.

Copyright information:

© 2016 Wiley Periodicals, Inc.

Export to EndNote