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Journal of Biomedicine and Biotechnology
Volume 2010 (2010), Article ID 724914, 10 pages
Research Article

Impaired Skeletal Muscle Repair after Ischemia-Reperfusion Injury in Mice

A. Vignaud,1,2,3,4 C. Hourde,1,2,3,4 F. Medja,1,2,3,4 O. Agbulut,5 G. Butler-Browne,1,2,3,4 and A. Ferry1,2,3,4,6

1INSERM, U974, Paris 75013, France
2Institut de Myologie, Paris 75013, France
3UMR S974, Université Pierre et Marie Curie-Paris6, Paris 75013, France
4CNRS UMR 7215, Paris 75013, France
5Unité de BFA/CNRS EAC 4413, Université Paris Diderot, Paris 75013, France
6Université Paris Descartes, Paris 75006, France

Received 18 December 2009; Accepted 2 March 2010

Academic Editor: Henk L. M. Granzier

Copyright © 2010 A. Vignaud et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Ischemia/reperfusion (IR) injury can induce skeletal muscle fibre death and subsequent regeneration. By 14 days, absolute and specific maximal forces and fatigue resistance in ischemic/reperfused soleus muscles were still reduced (−89%, −81%, and −75%, resp.) as compared to control muscles ( ). The decrease of these parameters in ischemic/reperfused muscle was much greater than that of myotoxic injured muscles (−12%, −11%, and −19%; ). In addition, at 14 days ischemic/reperfused muscle structure was still abnormal, showing small muscle fibres expressing neonatal myosin heavy chain and large necrotic muscle fibres that were not observed in myotoxin treated muscles. By 56 days, in contrast to myotoxin treated muscles, specific maximal force and muscle weight of the ischemic/reperfused muscles did not fully recover ( ). This differential recovery between ischemic/reperfused and myotoxin treated muscles was not related to the differences in the initial cell death, loss of satellite cells after injury, expression of growth factors (IGF1, IGF2..), or capillary density in regenerating muscles. In conclusion, our results demonstrate that IR injury in mice induces long term detrimental effects in skeletal muscles and that the recovery following IR injury was delayed for yet unknown reasons as compared to myotoxic injury.