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 receptor 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⁺ signaling, led to a fully restored heart function and structure, with skeletal muscle performance improvements, associated with a reduction in inflammation and senescence markers. Muscle NAD⁺ levels were also fully restored, while the levels of the two main products of CD38, nicotinamide and ADP-ribose, were reduced, in heart, diaphragm,

SUBMITTER: de Zelicourt A 

PROVIDER: S-EPMC9081905 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature