American researchers sought to better understand the function and effects of long-term corticosteroid therapy in Duchenne muscular dystrophy (DMD):
- the gene encoding the glucocorticoid receptor was invalidated in one of the animal models of DMD (the mdx52 mouse),
- the double knock-out mice thus created were studied from a physiological (strength and function measurements) and histological (skeletal muscle fibres and cardiomyocytes) point of view,
- the phenotype obtained was much more severe than that of the original mouse.
This work argues in favour of a protective effect of this receptor in the physiological state but also in the context of DMD, as observed in clinical trials.
