Literature DB >> 15193351

Erythropoietin: a new tool for muscle disorders?

C Scoppetta1, F Grassi.   

Abstract

The main action of erythropoietin (EPO) is to regulate the production of red cells. However both experimental evidence and clinical experience suggest that erythropoietin has a positive effect on skeletal and cardiac muscle. Mice lacking EPO or its receptors suffer from hearth hypoplasia and have a reduced number of proliferating cardiac myocytes. EPO receptors are expressed on mouse primary satellite cells and in cultured myoblasts, and their stimulation appears to enhance proliferation and reduce the differentiation of both cell types. Moreover EPO is capable of promoting angiogenesis in muscle cells, which provides an additional route to increase oxygen supply to active muscles. In men, the effects of EPO on muscle cells are suggested by the illegal use of EPO by agonistic and amateur athletes to enhance their performances. In some athletes EPO improved their long-duration muscular performances much more than expected on the basis of the increment of the blood hemoglobin alone. Our proposal is to investigate the effect of EPO treatment in various animal models of muscular dystrophies (MD), which are common hereditary primary muscle disorders characterized by muscle damage and wasting, to date without any effective treatment. The ability of EPO to induce the proliferation of satellite cells in the presence of differentiating conditions, typical of the damaged muscle, may represent a tool to expand the cellular population competent for muscle repair. This would lengthen the period when muscles can be efficiently repaired. In the presence of positive results, the possibility could be considered of selecting some of the human forms of MD and treating the patients with EPO.

Entities:  

Mesh:

Substances:

Year:  2004        PMID: 15193351     DOI: 10.1016/j.mehy.2003.12.044

Source DB:  PubMed          Journal:  Med Hypotheses        ISSN: 0306-9877            Impact factor:   1.538


  5 in total

1.  Three weeks of erythropoietin treatment hampers skeletal muscle mitochondrial biogenesis in rats.

Authors:  Vladimir E Martinez-Bello; Fabian Sanchis-Gomar; Marco Romagnoli; Frederic Derbre; Mari Carmen Gomez-Cabrera; Jose Viña
Journal:  J Physiol Biochem       Date:  2012-05-25       Impact factor: 4.158

2.  Carbamylated erythropoietin does not alleviate signs of dystrophy in mdx mice.

Authors:  Melissa P Wu; Emanuela Gussoni
Journal:  Muscle Nerve       Date:  2011-01       Impact factor: 3.217

3.  Skeletal muscle intrinsic functional properties are preserved in a model of erythropoietin deficient mice exposed to hypoxia.

Authors:  Luciana Hagström; Francis Canon; Onnik Agbulut; Dominique Marchant; Bernard Serrurier; Jean-Paul Richalet; Michèle Beaudry; Xavier Bigard; Thierry Launay
Journal:  Pflugers Arch       Date:  2010-01-30       Impact factor: 3.657

4.  Blunting effect of hypoxia on the proliferation and differentiation of human primary and rat L6 myoblasts is not counteracted by Epo.

Authors:  T Launay; L Hagström; S Lottin-Divoux; D Marchant; P Quidu; F Favret; A Duvallet; T Darribère; J P Richalet; M Beaudry
Journal:  Cell Prolif       Date:  2010-02       Impact factor: 6.831

5.  Erythropoietin reduces the expression of myostatin in mdx dystrophic mice.

Authors:  D Feder; M Rugollini; A Santomauro; L P Oliveira; V P Lioi; R dos Santos; L G Ferreira; M T Nunes; M H Carvalho; P O Delgado; A A S Carvalho; F L A Fonseca
Journal:  Braz J Med Biol Res       Date:  2014-09-05       Impact factor: 2.590

  5 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.