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Recent Patents on Regenerative Medicine

Volume 1 Issue 3
ISSN: 2210-2965
eISSN: 2210-2973

 

   All Titles

  Inhibitors of Myostatin- and Proteasome-Dependent Signaling for Attenuating Muscle Wasting
  pp.284-298 (15) Authors: Kunihiro Sakuma, Akihiko Yamaguchi
doi: 10.2174/10284
 
 
      Abstract

Myostatin is a major negative regulator of muscle mass. Interestingly, myostatin can modulate the expression and functional activity of myogenic regulatory factors such as MyoD and Forkhead BoxO (FOXO). Recently, Akt, a crucial enhancer of muscle hypertrophy, has been shown to interact with Smad2 and 3, downstream of a myostatin-dependent pathway. Ubiquitin-proteasome signaling is the most common system of protein degradation during rapid musclular atrophy after denervation, immobilization, or hindlimb suspension (unweighting) through the downstream mediator Atrogin-1 and FOXO. Deregulation of myostatin signaling has been implicated in the pathology of a number of major muscle wasting disorders including several muscular dystrophy, sarcopenia, cachexia, and amyotrophic lateral sclerosis. Worldwide, the pharmaceutical industry is actively developing better strategies for targeting muscle wasting, in particular, myostatin and proteasome-inhibitors. This patent review provides an overview of recent attempts to attenuate or inhibit muscle wasting using new and improved myostatin- and proteasome-linked agents. Proteasome inhibitor may not be appropriate for blocking muscle atrophy induced by sarcopenia and cachexia.

 
  Keywords: Muscular dystrophy, muscle wasting, myostatin, proteasome, sarcopenia, skeletal muscle, Cachexia, Amyotrophic Lateral Sclerosis (ALS), Myostatin Inhibition, UBIQUITIN-PROTEASOME SYSTEM
  Affiliation: Research Center for Physical Fitness, Sports and Health, Toyohashi, University of Technology, 1-1 Hibarigaoka, Tenpaku-cho, Toyohashi, 441-8580, Japan.
 
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