|
|
||||||||
1 Internal Medicine, City Hospital, 45011 Adria; 2 Consiglio Nazionale delle Ricerche Institute of Neuroscience, Unit for Muscle Biology and Pathophysiology, Department of Biomedical Sciences, and 3 Department of Cardiovascular Pathology, University of Padua, 35100 Padua; 4 Department of Experimental Oncology, National Cancer Institute, 80072 Naples; 5 Scientific Department, Sigma Tau, 00040 Rome, Italy
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.
tumor necrosis factor; sphingosine; caspases; staurosporine
This article has been cited by other articles:
![]() |
B. T. Steffen, S. J. Lees, and F. W. Booth Anti-TNF treatment reduces rat skeletal muscle wasting in monocrotaline-induced cardiac cachexia J Appl Physiol, December 1, 2008; 105(6): 1950 - 1958. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. A Calo, P. A Davis, E. Pagnin, L. Bertipaglia, A. Naso, A. Piccoli, R. Corradini, M. Spinello, V. Savica, and L. D. Libera Carnitine-mediated improved response to erythropoietin involves induction of haem oxygenase-1: studies in humans and in an animal model Nephrol. Dial. Transplant., March 1, 2008; 23(3): 890 - 895. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. Vescovo, B. Ravara, V. Gobbo, and L. D. Libera Inflammation and perturbation of the L-carnitine system in heart failure Eur J Heart Fail, October 1, 2005; 7(6): 997 - 1002. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. Schreiber Levocarnitine and Dialysis: A Review Nutr Clin Pract, April 1, 2005; 20(2): 218 - 243. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Ventura-Clapier, A. Garnier, and V. Veksler Energy metabolism in heart failure J. Physiol., February 15, 2004; 555(1): 1 - 13. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Dalla Libera, B. Ravara, M. Volterrani, V. Gobbo, M. Della Barbera, A. Angelini, D. D. Betto, E. Germinario, and G. Vescovo Beneficial effects of GH/IGF-1 on skeletal muscle atrophy and function in experimental heart failure Am J Physiol Cell Physiol, January 1, 2004; 286(1): C138 - C144. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Selman and C. Leeuwenburgh The role of Id2 and apoptosis during skeletal muscle remodeling Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2003; 284(2): R538 - R539. [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |