The CD38-NADase is a new major contributor to Duchenne muscular dystrophic phenotype

ABSTRACT: Duchenne muscular dystrophy (DMD) is characterized by progressive muscle degeneration. Two important deleterious features are a Ca2+ dysregulation linked to Ca2+ influxes associated with ryanodine receptors hyperactivation, and a muscular nicotinamide adenine dinucleotide (NAD+) deficit. Here, we identified that deletion in mdx mice of CD38, a NAD+ glycohydrolase producing modulators of Ca2+ signalling, led to a fully restored heart function and structure, with skeletal muscle performance improvements, associated with a reduction of inflammation and senescence markers. Muscle NAD+ levels were also fully restored while the levels of the two main products of CD38, nicotinamide and APDribose were reduced, in heart, diaphragm, and limb. In cardiomyocytes from mdx/CD38-/- mice, the pathologica

SUBMITTER: Dr. Antoine de Zelicourt 

PROVIDER: S-SCDT-EMM-2020-12860 | biostudies-other |

REPOSITORIES: biostudies-other