Caveolae: A regulatory platform for nutritional modulation of inflammatory diseases

Joseph Layne, Zuzana Majkova, Eric J. Smart, Michal Toborek, Bernhard Hennig

Research output: Contribution to journalArticle

27 Scopus citations

Abstract

Dietary intervention strategies have proven to be an effective means of decreasing several risk factors associated with the development of atherosclerosis. Endothelial cell dysfunction influences vascular inflammation and is involved in promoting the earliest stages of lesion formation. Caveolae are lipid raft microdomains abundant within the plasma membrane of endothelial cells and are responsible for modulating receptor-mediated signal transduction, thus influencing endothelial activation. Caveolae have been implicated in the regulation of enzymes associated with several key signaling pathways capable of determining intracellular redox status. Diet and plasma-derived nutrients may modulate an inflammatory outcome by interacting with and altering caveolae-associated cellular signaling. For example, omega-3 fatty acids and several polyphenolics have been shown to improve endothelial cell function by decreasing the formation of ROS and increasing NO bioavailability, events associated with altered caveolae composition. Thus, nutritional modulation of caveolae-mediated signaling events may provide an opportunity to ameliorate inflammatory signaling pathways capable of promoting the formation of vascular diseases, including atherosclerosis.

Original languageEnglish (US)
Pages (from-to)807-811
Number of pages5
JournalJournal of Nutritional Biochemistry
Volume22
Issue number9
DOIs
StatePublished - Sep 1 2011
Externally publishedYes

Keywords

  • Caveolae
  • Inflammatory diseases
  • Nutritional modulation

ASJC Scopus subject areas

  • Biochemistry
  • Clinical Biochemistry
  • Molecular Biology
  • Endocrinology, Diabetes and Metabolism
  • Nutrition and Dietetics

Fingerprint Dive into the research topics of 'Caveolae: A regulatory platform for nutritional modulation of inflammatory diseases'. Together they form a unique fingerprint.

  • Cite this