Vascular signaling through cholesterol-rich domains: implications in hypertension

Curr Opin Nephrol Hypertens. 2007 Mar;16(2):90-104. doi: 10.1097/MNH.0b013e328040bfbd.

Abstract

Purpose of review: Lipid rafts are emerging as key players in the integration of cellular responses. Alterations in these highly regulated signaling cascades are important in structural, mechanical and functional abnormalities that underlie vascular pathological processes. The present review focuses on recent advances in signal transduction through caveolae/lipid rafts, implicated in hypertensive processes.

Recent findings: Caveolae/lipid rafts function as sites of dynamic regulatory events in receptor-induced signal transduction. Mediators of vascular function, including G-protein coupled receptors, Src family tyrosine kinases, receptor tyrosine kinases, protein phosphatases and nitric oxide synthase, are concentrated within these microdomains. The assembly of functionally active nicotinamide adenine dinucleotide phosphate oxidase and subsequent reactive oxygen species production are also dependent on interactions within the caveolae/lipid rafts. Recent findings have also demonstrated the importance of actin-cytoskeleton and focal adhesion sites for protein interactions with caveolae/lipid raft.

Summary: Many vascular signaling processes are altered in hypertension. Whether these events involve lipid rafts/caveolae remains unclear. A better understanding of how signaling molecules compartmentalize in lipid rafts/caveolae will provide further insights into molecular mechanisms underlying vascular damage in cardiovascular disease.

Publication types

  • Review

MeSH terms

  • Caveolae / physiology
  • ErbB Receptors / physiology
  • Humans
  • Hypertension / physiopathology*
  • Membrane Microdomains / physiology*
  • Nitric Oxide Synthase / metabolism
  • Protein Tyrosine Phosphatases / physiology
  • Signal Transduction / physiology*
  • Superoxides / metabolism
  • src-Family Kinases / physiology

Substances

  • Superoxides
  • Nitric Oxide Synthase
  • ErbB Receptors
  • src-Family Kinases
  • Protein Tyrosine Phosphatases