{"doi":"10.15252/emmm.202012860","title":"CD38‐NADase is a new major contributor to Duchenne muscular dystrophic phenotype","abstract":"Abstract Duchenne muscular dystrophy (DMD) is characterized by progressive muscle degeneration. Two important deleterious features are a Ca 2+ dysregulation linked to Ca 2+ 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 Ca 2+ 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, and limb. In cardiomyocytes from mdx/CD38 −/− mice, the pathological spontaneous Ca 2+ activity was reduced, as well as in myotubes from DMD patients treated with isatuximab (SARCLISA ® ) a monoclonal anti‐CD38 antibody. Finally, treatment of mdx and utrophin–dystrophin‐deficient ( mdx/utr −/− ) mice with CD38 inhibitors resulted in improved skeletal muscle performances. Thus, we demonstrate that CD38 actively contributes to DMD physiopathology. We propose that a selective anti‐CD38 therapeutic intervention could be highly relevant to develop for DMD patients.","journal":"EMBO Molecular Medicine","year":2022,"id":255214,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":20,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.96,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2022-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":902938,"name":"Abdallah Fayssoil","orcid":"0000-0003-3844-5438","position":1,"is_corresponding":false},{"id":902939,"name":"Mbarka Dakouane‐Giudicelli","orcid":"0000-0002-0169-0037","position":2,"is_corresponding":false},{"id":903453,"name":"Isley de Jesus","orcid":null,"position":3,"is_corresponding":false},{"id":900737,"name":"Ahmed Karoui","orcid":"0009-0005-4028-8445","position":4,"is_corresponding":false},{"id":902940,"name":"Faouzi Zarrouki","orcid":"0000-0003-0905-9036","position":5,"is_corresponding":false},{"id":902941,"name":"Florence Lefebvre","orcid":"0000-0003-0133-5825","position":6,"is_corresponding":false},{"id":902942,"name":"Arnaud Mansart","orcid":"0000-0003-1442-8924","position":7,"is_corresponding":false},{"id":902943,"name":"Jean‐Marie Launay","orcid":"0000-0003-4809-1020","position":8,"is_corresponding":false},{"id":902944,"name":"Jérôme Piquereau","orcid":"0000-0002-6019-8683","position":9,"is_corresponding":false},{"id":697303,"name":"Mariana G. 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