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Fetal-Like Slow Na+ Channels in Duchenne’s Muscular Dystrophy

  • Ghassan Bkaily
  • Adrian Sculptoreanu
  • Gaétan Jasmin
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 159)

Abstract

DMD is one of the most common and severest form of SM dystrophy that affects humans (for review see 16, 17). The basic problem in DMD is the lack of knowledge of the causes of the disease and the exact nature of events during initiation and progression of the segmental necrosis as a result, patients with DMD still face a break future (16). Increased [Ca]i in DMD has been well established. If it were known what caused this increase of [Ca]i, whether it be accelerated transport through voltage-dependent channels, alteration in Na+, or the activity of sarcolemmal Ca-ATPs, it would then be possible to develop specific drugs to prevent the accumulation of Ca2+ ions. Increased [Ca]i could stimulate several pathways including certain proteases, phospholipase A2 and calmodulin (which increases in dystrophic muscle) (18). The latter was reported to activate Ca2+ channel in heart (19).

Keywords

Muscular Dystrophy Voltage Step Embryonic Heart Slow Channel Human Myotube 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1994

Authors and Affiliations

  • Ghassan Bkaily
    • 1
    • 2
  • Adrian Sculptoreanu
    • 1
    • 2
  • Gaétan Jasmin
    • 1
    • 2
  1. 1.Department of Physiology and Biophysics, Faculty of MedicineUniversity of SherbrookeSherbrookeCanada
  2. 2.Department of Pathology, Faculty of MedicineUniversity of MontrealMontrealCanada

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