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Angiotensin II, oxidative stress and skeletal muscle wasting.

Authors
  • Sukhanov, Sergiy1
  • Semprun-Prieto, Laura
  • Yoshida, Tadashi
  • Michael Tabony, A
  • Higashi, Yusuke
  • Galvez, Sarah
  • Delafontaine, Patrice
  • 1 Tulane University Heart and Vascular Institute, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Type
Published Article
Journal
The American journal of the medical sciences
Publication Date
Aug 01, 2011
Volume
342
Issue
2
Pages
143–147
Identifiers
DOI: 10.1097/MAJ.0b013e318222e620
PMID: 21747283
Source
Medline
License
Unknown

Abstract

Muscle atrophy (cachexia) is a muscle wasting syndrome associated with several pathological conditions in humans such as congestive heart failure, diabetes, AIDS, cancer and renal failure, and the presence of cachexia worsens outcome. Many of the conditions associated with cachexia are accompanied by stimulation of the renin-angiotensin system and elevation in angiotensin II (ang II) levels. Ang II infusion induces skeletal muscle atrophy in rodents and mechanisms include increased expression of the E3 ligases atrogin-1/MuRF-1, an elevated rate of ubiquitin-proteasome mediated proteolysis and increased reactive oxygen species (ROS) levels, closely mimicking conditions of human cachexia. Ang II-induced oxidative stress contributes to muscle atrophy in a mouse model. Nicotinamide adenine dinucleotide phosphate oxidase- and mitochondria-derived ROS contribute to ang II-induced oxidative stress. Specific targeting of ROS and nicotinamide adenine dinucleotide phosphate oxidase/mitochondria cross-talk could be a beneficial, novel therapy to treat cachexia.

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