Actually, muscle tissues growth and repair is impelled by the stem cells present inside it. By recognizing the mechanism that activates muscle stem cells to perform their task, new ways could be discovered to enhance muscle growth. However, the activation systems are not clearly understood.
Now, researchers from Sanford Burnham Prebys Institute have identified a molecular signaling pathway associated with Stat3 and Fam3a proteins that control the decision opted by muscle stem cells either to differentiate or self-renew. By using this approach, several muscular dystrophies or age-related muscle decline conditions could be cured. The research has appeared in the journal Nature Communications.
After a certain age, the efficiency of muscle stem cells to regenerate tissues enters the declining phase due to the natural aging process, known as sarcopenia, or any type of chronic muscle disease. The researchers have worked over it and found drug targets, which could give promising results by directing muscle stem cells to follow the correct pathway of tissue repair. This could facilitate significant depletion of the symptoms that generally appear during aging and muscular dystrophy.
Muscle exhaustion occurs due to sarcopenia and genetic syndrome such as muscular dystrophies. Almost 10% of adults crossed 50 and around half of the aged people in their 80s are affected by sarcopenia. Muscular dystrophies comprise over 30 genetic diseases that lead to muscle weakness and deterioration. At present, no cure has been there for muscular dystrophy.
The study conducted by the researchers on mouse models revealed that Stat3 protein regulates several cellular processes including mitochondrial respiration. The researchers identified specific genes that expressed along with Stat3 during muscle growth to uncover additional proteins that might be used as targets in therapeutic treatment. They found that Fam3a protein-generating gene was also expressed.
To uncover the role of Fam3a protein, the researchers developed cell lines and mouse strain in which Fam3a gene was absent. The experiment concluded that protein is essential for both muscle growth and muscle stem cell differentiation. Therefore, by targeting the specific gene using therapeutic techniques, the symptoms of muscular dystrophy can be declined.
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