Apoptosis in the Skeletal Muscle of Rats with Heart Failure is Associated with Increased Serum Levels of TNF-α and Sphingosine

Skeletal muscle in congestive heart failure (CHF) is responsible for increased fatigability, decreased endurance and exercise capacity. A specific myopathy with increased expression of fast myosin heavy chains (MHCs), myocyte atrophy, secondary to myocyte apoptosis, that is triggered by high levels...

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Bibliographic Details
Published in:Journal of molecular and cellular cardiology 2001-10, Vol.33 (10), p.1871-1878
Main Authors: Dalla Libera, Luciano, Sabbadini, Roger, Renken, Christian, Ravara, Barbara, Sandri, Marco, Betto, Romeo, Angelini, Annalisa, Vescovo, Giorgio
Format: Article
Language:English
Subjects:
Angiotensin II - biosynthesis
Animals
Apoptosis
Blotting, Western
Cells, Cultured
Chromatography, High Pressure Liquid
Dose-Response Relationship, Drug
Heart failure
Heart Failure - metabolism
Heart Ventricles - pathology
Hypertrophy, Right Ventricular - pathology
In Situ Nick-End Labeling
Male
Muscle, Skeletal - metabolism
Muscle, Skeletal - pathology
Rats
Rats, Sprague-Dawley
Skeletal muscle
Sphingosine
Sphingosine - blood
Sphingosine - metabolism
Tumor Necrosis Factor-alpha - metabolism
Tumor necrosis factor-α
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Summary:Skeletal muscle in congestive heart failure (CHF) is responsible for increased fatigability, decreased endurance and exercise capacity. A specific myopathy with increased expression of fast myosin heavy chains (MHCs), myocyte atrophy, secondary to myocyte apoptosis, that is triggered by high levels of circulating tumor necrosis factor (TNF- α) has been described. However, a direct effect of TNF- α on skeletal muscle has not been described yet. In this paper we put forward the hypothesis that TNF- α plays an indirect effect on skeletal myocytes. In an animal model of CHF, the monocrotaline-treated rat, we have observed a significant (P
ISSN:0022-2828
1095-8584
DOI:10.1006/jmcc.2001.1453