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Redox signaling in cardiovascular health and disease.

Abstract
Spatiotemporal regulation of the activity of a vast array of intracellular proteins and signaling pathways by reactive oxygen species (ROS) governs normal cardiovascular function. However, data from experimental and animal studies strongly support that dysregulated redox signaling, resulting from hyperactivation of various cellular oxidases or mitochondrial dysfunction, is integral to the pathogenesis and progression of cardiovascular disease (CVD). In this review, we address how redox signaling modulates the protein function, the various sources of increased oxidative stress in CVD, and the labyrinth of redox-sensitive molecular mechanisms involved in the development of atherosclerosis, hypertension, cardiac hypertrophy and heart failure, and ischemia-reperfusion injury. Advances in redox biology and pharmacology for inhibiting ROS production in specific cell types and subcellular organelles combined with the development of nanotechnology-based new in vivo imaging systems and targeted drug delivery mechanisms may enable fine-tuning of redox signaling for the treatment and prevention of CVD.
AuthorsNageswara R Madamanchi, Marschall S Runge
JournalFree radical biology & medicine (Free Radic Biol Med) Vol. 61 Pg. 473-501 (Aug 2013) ISSN: 1873-4596 [Electronic] United States
PMID23583330 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Review)
CopyrightCopyright © 2013 Elsevier Inc. All rights reserved.
Chemical References
  • Reactive Oxygen Species
  • Transcription Factors
  • Protein Kinases
  • PTPN1 protein, human
  • Protein Tyrosine Phosphatase, Non-Receptor Type 1
Topics
  • Animals
  • Cardiovascular Diseases (etiology, metabolism)
  • Cardiovascular System (metabolism)
  • Humans
  • Mitochondria (metabolism)
  • Oxidation-Reduction
  • Protein Kinases (physiology)
  • Protein Tyrosine Phosphatase, Non-Receptor Type 1 (physiology)
  • Reactive Oxygen Species (metabolism)
  • Transcription Factors (physiology)

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