Effect of thalidomide on the skeletal muscle in experimental heart failure

Giorgio Vescovo, Barbara Ravara, Annalisa Angelini, Marco Sandri, Ugo Carraro, Claudio Ceconi, Luciano Dalla Libera

Research output: Contribution to journalArticlepeer-review


Background: Tumour Necrosis Factor α (TNFα) has been shown to contribute to heart failure (CHF) progression. Aims: We have tried to antagonise the detrimental effects of TNFα on skeletal muscle apoptosis, by using thalidomide, a drug that inhibits its biosynthesis. Methods: CHF was induced in 20 rats by injecting monocrotaline, which determines right ventricle (RV) failure. After 2 weeks, when CHF developed, 12 rats were treated with thalidomide 3.5.mg/kg per day for 2 weeks. Eight had saline and served as CHF controls. Results: Thalidomide failed to decrease TNFα and its second messenger sphingosine (SPH), but was able to prevent the shift toward the fast myosin heavy chains. In the Tibialis Anterior muscle of the thalidomide group, the degree of atrophy, the number of apoptotic nuclei and the levels of caspases, were similar to those of the CHF controls. Conclusions: Thalidomide, at the doses used in this study, which are the same employed for the treatment of tubercolosis, leprosy, AIDS and cancer in humans, did not lower either TNFα or SPH and only marginally influenced the apoptosis-induced muscle atrophy. Since other TNFα blockers are under investigation for improving the clinical status of patients with CHF, the present data could be relevant in the design of randomised clinical trials in humans.

Original languageEnglish
Pages (from-to)455-460
Number of pages6
JournalEuropean Journal of Heart Failure
Issue number4
Publication statusPublished - Aug 1 2002


  • Apoptosis
  • Cytokines
  • Heart failure
  • Skeletal muscle
  • Sphingosine
  • TNFα

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


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