Newly discovered mechanisms lay the foundation for a new therapeutic avenues that one day may be beneficial in treating diseases, ranging from muscle weakness and frailty to obesity and diabetes.
Researchers from EPFL published a study which highlight on the roles of a nuclear receptor co-repressor, NCoR1. Very little is known about how co-repressors, which inhibit gene transcription function and hence brake gene expression, work in the animal. In two independent studies now investigators address the function of the co-repressor NCoR1 in two different tissues, muscle and fat tissue. Interestingly, the absence of NCoR1 in muscle or adipose tissue leads to improved function of both tissues.
In the muscle the absence of NCoR1 leads to increased muscle mass, as you would expect if you omit an inhibitory factor. Interestingly, NCoR1 not only inhibits muscle mass but also seems to inhibit muscle function. Animals that lack NCoR1 in the muscle become really super performers - “marathon” animals - and move better and significantly longer. The research team showed that this effect of NCoR1 is remarkably conserved in evolution from worms to mice. “Inhibitors of NCoR1 function could hence be of value to treat diseases with impaired muscle function, subsequent to genetic mutations, such as muscle dystrophy”, comments Hiroyasu Yamamoto, researcher at EPFL and author of the study. Auwerx, researcher as well, points to another perhaps more important indication, muscle weakness also known as frailty, the prime cause of falling in the elderly. “We are actively screening to identify compounds and drugs that inhibit NCoR1 to treat these muscle disease” comments Auwerx.
These newly discovered mechanisms by which NCoR1 functions hence lays the foundation for a new therapeutic avenues that one day may be beneficial in treating diseases, ranging from muscle weakness and frailty to obesity and diabetes.