Journal
AMERICAN JOURNAL OF THE MEDICAL SCIENCES
Volume 342, Issue 2, Pages 143-147Publisher
ELSEVIER SCIENCE INC
DOI: 10.1097/MAJ.0b013e318222e620
Keywords
Angiotensin II; Muscle atrophy; Oxidative stress
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Funding
- NHLBI NIH HHS [R01 HL070241, R01 HL070241-08, R01 HL080682, R01 HL080682-05] Funding Source: Medline
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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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