MDA Resource Center: We’re Here For You
Our trained specialists are here to provide one-on-one support for every part of your journey. Send a message below or call us at 1-833-ASK-MDA1 (1-833-275-6321). If you live outside the U.S., we may be able to connect you to muscular dystrophy groups in your area, but MDA programs are only available in the U.S.
NF-kB signaling in muscle regeneration and disease

The NF-kB pathways form a signaling complex that is critical for normal skeletal muscle function and is important in promoting recovery in response to muscle injury. Furthermore, there is strong evidence that prolonged NF-kB activation is detrimental to normal skeletal muscle function and can contribute to diseases such as the common genetic disorder, Duchenne muscular dystrophy (DMD). As such, NF-kB has become an attractive drug target for the treatment of muscle diseases. It has been shown that cellular inhibitor of apoptosis 1, cIAP1, can modify NF-kB signaling in skeletal muscle in a beneficial manner. This discovery has raised the exciting possibility that cIAP1 may be a potential therapeutic target for various muscle diseases that are caused or worsened by prolonged NF-kB signaling. Since there are several drugs and reagents that potently and specifically eliminate cIAP1 expression, I will evaluate their therapeutic potential in mdx mice, the mouse model for DMD. I will also clarify the role that cIAP1 plays in the disordered muscle structure and function associated with DMD and how cIAP1 regulates NF-kB signaling in dystrophic muscle. Findings from this study have the potential to improve muscle structure and function and thus the quality of life of patients living with DMD.
Institution: Children's Hospital of Eastern Ontario Research Institute Inc
Institution Country: Canada
https://doi.org/10.55762/pc.gr.157031
Grantee: Neena Lala-Tabbert, Ph.D.
Grant type: Development Grant
Award total: $199,842.22
Institution: Children's Hospital of Eastern Ontario Research Institute Inc
Country: Canada