The research was published in the Journal of Clinical Investigation, and describes the role of TNF receptor-associated factor 6, an adaptor protein and E3 ubiquitin ligase, in ensuring the vitality of stem cells that regenerate muscle tissue.
In their research, authors Sajedah M. Hindi, PhD, and Ashok Kumar, PhD, discovered that removing TRAF6 depletes Pax7, resulting on reduced muscle regeneration in both normal and Duchenne muscular dystrophy mouse models. The researchers believe this is because TRAF6 is upstream from Pax7 in the signaling process involved in muscle repair and orchestrates multiple signals controlling the muscle regeneration process.
Here are four observations:
1. Dr. Kumar said they have discovered a pathway by which the Pax7 and myogenic potential of satellite cells is regulated. The protein TRAF6 is a very important adaptor protecin that is involved in multiple signaling pathways and its functions are important to maintain the stemness of satellite in cells in adults.
2. Dr. Hindi said in normal conditions, skeletal muscle is a self-healing tissue and can recover promptly from most trauma because of the satellite cells, but in disease conditions like muscular dystrophies, satellite cells can’t keep up with repeated cycles of injury and are ultimately exhausted or functionally impaired.
3. According to Dr. Hindi, their next step is to see if this functional impairment is partially due to lack of TRAF6 signaling in satellite cells, and if so, they are thinking they can take a patient’s stem cells, restore the TRAF6 activity and put them back and boost their regenerative potential.
4. Dr. Kumar and Dr. Hindi believe their research ultimately will lead to improved treatments for muscle wasting diseases such as muscular dystrophy, ALS, cancer cachexia, diabetes, heart disease and others.
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