MSGID: 1:317/3 646ee47d   
   PID: hpt/lnx 1.9.0-cur 2019-01-08   
   TID: hpt/lnx 1.9.0-cur 2019-01-08   
    Discovery slows down muscular dystrophy    
    University of Houston researchers target protein that can slow disease   
   progression, improve muscle function    
      
     Date:   
         May 24, 2023   
     Source:   
         University of Houston   
     Summary:   
         A research team has discovered that by manipulating a certain   
         protein in the immune system they can slow down disease progression   
         and improve muscle function in Duchenne muscular dystrophy.   
      
      
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   FULL STORY   
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   A team of researchers at the University of Houston College of Pharmacy is   
   reporting that by manipulating TAK1, a signaling protein that plays an   
   important role in development of the immune system, they can slow down   
   disease progression and improve muscle function in Duchenne muscular   
   dystrophy (DMD).   
      
   DMD, caused by mutations in dystrophin gene, is an inheritable   
   neuromuscular disorder that occurs in one out of 3,600 male births. DMD   
   patients undergo severe muscle wasting, inability to walk and eventually   
   death in their early thirties due to respiratory failure. The disease is   
   marked by an inflammatory response and death of muscle fibers. Eventually,   
   the muscle fibers are replaced with fat and fibrotic tissue that causes   
   severe muscle weakness.   
      
   "Our results suggest that TAK1 (transforming growth factor b-activated   
   kinase1) is a regulator of skeletal muscle mass. By specifically   
   targeting this protein, we can suppress the death of muscle fibers,   
   known as myonecrosis, and slow down disease progression in DMD," said   
   Ashok Kumar, Else and Philip Hargrove Endowed Professor and chair,   
   Department of Pharmacological and Pharmaceutical Sciences, whose results   
   were published in JCI Insight. "Our research shows that activating TAK1   
   can stimulate myofiber growth in a model of DMD, with no negative impact   
   on muscle health."  In a previous breakthrough, Kumar's team uncovered   
   a surprising fact: TAK1 is essential for maintaining skeletal muscle   
   mass and that activating TAK1 beyond normal levels can enhance skeletal   
   muscle growth.   
      
   For this research, supported by the National Institutes of Health,   
   the team designed experiments to reduce or augment the levels of TAK1   
   protein in skeletal muscle at different stages of disease progression.   
      
   "Our experiments demonstrate that depletion of TAK1 activity during peak   
   necrotic phase followed by re-introduction of TAK1 at post-necrotic phase   
   leads to substantial improvement in muscle pathology," said Anirban Roy,   
   research assistant professor.   
      
   The current standard of care for DMD is focused on reducing inflammation   
   with corticosteroids, which modestly reduces disease progression, but   
   has serious side effects.   
      
   "Accumulating evidence suggests that regulation of immune response,   
   autophagy, and metabolism along with gene correction therapy can be   
   promising approaches to slow down disease progression in DMD patients,"   
   said Roy.   
      
       * RELATED_TOPICS   
             o Health_&_Medicine   
                   # Muscular_Dystrophy # Fibromyalgia # Fitness #   
                   Chronic_Illness # Joint_Pain # Neuropathy # Healthy_Aging   
                   # Human_Biology   
       * RELATED_TERMS   
             o Immune_system o AIDS o Protein o Physical_exercise o Meat   
             o Blood_vessel o Botulinum_toxin_(cosmetic_treatment) o Artery   
      
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   Story Source: Materials provided by University_of_Houston. Original   
   written by Laurie Fickman. Note: Content may be edited for style and   
   length.   
      
      
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   Journal Reference:   
      1. Anirban Roy, Tatiana E. Koike, Aniket S. Joshi, Meiricris Tomaz   
      da Silva,   
         Kavya Mathukumalli, Mingfu Wu, Ashok Kumar. Targeted regulation   
         of TAK1 counteracts dystrophinopathy in a DMD mouse model. JCI   
         Insight, 2023; 8 (10) DOI: 10.1172/jci.insight.164768   
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   Link to news story:   
   https://www.sciencedaily.com/releases/2023/05/230524181848.htm   
      
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