{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["de Zelicourt A"],"funding":["Agence Nationale de la Recherche","NIA NIH HHS","Foundation for the National Institutes of Health","Fondation de France"],"pagination":["e12860"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9081905"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(5)"],"pubmed_abstract":["Duchenne muscular dystrophy (DMD) is characterized by progressive muscle degeneration. Two important deleterious features are a Ca<sup>2+</sup> dysregulation linked to Ca<sup>2+</sup> influxes associated with ryanodine receptor hyperactivation, and a muscular nicotinamide adenine dinucleotide (NAD<sup>+</sup> ) deficit. Here, we identified that deletion in mdx mice of CD38, a NAD<sup>+</sup> glycohydrolase-producing modulators of Ca<sup>2+</sup> 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<sup>+</sup> levels were also fully restored, while the levels of the two main products of CD38, nicotinamide and ADP-ribose, were reduced, in heart, diaphragm,"],"journal":["EMBO molecular medicine"],"pubmed_title":["CD38-NADase is a new major contributor to Duchenne muscular dystrophic phenotype."],"pmcid":["PMC9081905"],"funding_grant_id":["ANR‐10‐LABX‐33","R01 AG058812","AG58812","ANR‐19‐CE14‐0031‐01","NAD‐Heart # 17‐CE17‐0015‐01","00086505","ANR‐13‐BSV1‐0023‐01"],"pubmed_authors":["Dakouane-Giudicelli M","Pietri-Rouxel F","Bonay M","Piquereau J","Chini EN","Lefebvre F","Chini CCS","Fogarty MJ","Cancela JM","Forand A","De Jesus I","Brisebard E","Mericskay M","Launay JM","Tarrago MG","Karoui A","Zarrouki F","Sieck GC","de la Porte S","Kashyap S","Mansart A","Moog S","de Zelicourt A","Gomez AM","Fayssoil A"],"additional_accession":[]},"is_claimable":false,"name":"CD38-NADase is a new major contributor to Duchenne muscular dystrophic phenotype.","description":"Duchenne muscular dystrophy (DMD) is characterized by progressive muscle degeneration. Two important deleterious features are a Ca<sup>2+</sup> dysregulation linked to Ca<sup>2+</sup> influxes associated with ryanodine receptor hyperactivation, and a muscular nicotinamide adenine dinucleotide (NAD<sup>+</sup> ) deficit. Here, we identified that deletion in mdx mice of CD38, a NAD<sup>+</sup> glycohydrolase-producing modulators of Ca<sup>2+</sup> 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<sup>+</sup> levels were also fully restored, while the levels of the two main products of CD38, nicotinamide and ADP-ribose, were reduced, in heart, diaphragm,","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 May","modification":"2025-04-19T12:09:13.824Z","creation":"2025-02-19T00:55:35.589Z"},"accession":"S-EPMC9081905","cross_references":{"pubmed":["35298089"],"doi":["10.15252/emmm.202012860"]}}