Loading…

L-Carnitine: a potential treatment for blocking apoptosis and preventing skeletal muscle myopathy in heart failure

Skeletal muscle in congestive heart failure is responsible for increased fatigability and decreased exercise capacity. A specific myopathy with increased expression of fast-type myosins, myocyte atrophy, secondary to myocyte apoptosis triggered by high levels of circulating tumor necrosis factor- (T...

Full description

Saved in:
Bibliographic Details
Published in:American Journal of Physiology: Cell Physiology 2002-09, Vol.52 (3), p.C802-C810
Main Authors: VESCOVO, Giorgio, RAVARA, Barbara, DALLA LIBERA, Luciano, GOBBO, Valerio, SANDRI, Marco, ANGELINI, Annalisa, DELLA BARBERA, Mila, DONA, Massimo, PELUSO, Gianfranco, CALVANI, Menotti, MOSCONI, Luigi
Format: Article
Language:English
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Skeletal muscle in congestive heart failure is responsible for increased fatigability and decreased exercise capacity. A specific myopathy with increased expression of fast-type myosins, myocyte atrophy, secondary to myocyte apoptosis triggered by high levels of circulating tumor necrosis factor- (TNF-) has been described. In an animal model of heart failure, the monocrotaline-treated rat, we have observed an increase of apoptotic skeletal muscle nuclei. Proapoptotic agents, caspase-3 and -9, were increased, as well as serum levels of TNF- and its second messenger sphingosine. Treatment of rats with L-carnitine, known for its protective effect on muscle metabolism injuries, was found to inhibit caspases and to decrease the levels of TNF- and sphingosine, as well as the number of apoptotic myonuclei. Staurosporine was used in in vitro experiments to induce apoptosis in skeletal muscle cells in culture. When L-carnitine was applied to skeletal muscle cells, before staurosporine treatment, we observed a reduction in apoptosis. These findings show that L-carnitine can prevent apoptosis of skeletal muscles cells and has a role in the treatment of congestive heart failure-associated myopathy.
ISSN:0363-6143
1522-1563