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Angiotensin II, oxidative stress and skeletal muscle wasting.
- Source :
-
The American journal of the medical sciences [Am J Med Sci] 2011 Aug; Vol. 342 (2), pp. 143-7. - Publication Year :
- 2011
-
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.
- Subjects :
- Angiotensin II metabolism
Animals
Humans
Mice
Mitochondria, Muscle metabolism
Mitochondria, Muscle physiology
Muscular Atrophy physiopathology
NADPH Oxidases metabolism
Reactive Oxygen Species metabolism
Receptors, Angiotensin metabolism
Receptors, Angiotensin physiology
Angiotensin II physiology
Muscular Atrophy metabolism
Oxidative Stress physiology
Subjects
Details
- Language :
- English
- ISSN :
- 1538-2990
- Volume :
- 342
- Issue :
- 2
- Database :
- MEDLINE
- Journal :
- The American journal of the medical sciences
- Publication Type :
- Academic Journal
- Accession number :
- 21747283
- Full Text :
- https://doi.org/10.1097/MAJ.0b013e318222e620