{"doi":"10.1016/j.ydbio.2025.09.022","title":"A zebrafish model of nicotinamide adenine dinucleotide (NAD+) deficiency-derived congenital disorders","abstract":"Developmental NAD + deficiency is associated with diverse congenital malformations. Congenital NAD deficiency disorder (CNDD) is a multisystem developmental condition characterized by cardiac, renal, vertebral, and limb anomalies, among others. It is caused by biallelic pathogenic variants in genes involved in the nicotinamide adenine dinucleotide (NAD + ) synthesis pathway. CNDD anomalies overlap with clinical features described in vertebral-anal-cardiac-tracheoesophageal fistula-renal-limb (VACTERL) association, suggesting a possible shared etiological link through NAD + deficiency. However, the aberrant developmental mechanisms of NAD + -deficient congenital anomalies remain poorly understood. To dynamically explore NAD + -deficiency-induced congenital malformations, we developed a zebrafish model of NAD + disruption. Zebrafish embryos treated with 2-amino-1,3,4-thiadiazole (ATDA), a known NAD + metabolism disruptor, exhibited cardiac, tail, spinal cord, and craniofacial defects, which were partially rescued by nicotinamide (NAM) in a dose-dependent manner. Our work establishes zebrafish as a useful model for investigating how NAD + deficiency contributes to multisystem congenital anomalies.","journal":"Developmental Biology","year":2025,"id":576404,"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":0,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9435,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2025-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1256090,"name":"Carla Gilliland","orcid":null,"position":1,"is_corresponding":false},{"id":1256089,"name":"Jessica Ensing","orcid":null,"position":2,"is_corresponding":false},{"id":669228,"name":"Elizabeth VanSickle","orcid":"0000-0001-5504-9248","position":3,"is_corresponding":false},{"id":797340,"name":"Nathan Lanning","orcid":"0000-0002-0983-7451","position":4,"is_corresponding":false},{"id":434524,"name":"Paul R. Mark","orcid":"0000-0002-1020-888X","position":5,"is_corresponding":false},{"id":411224,"name":"Stephanie Grainger","orcid":"0000-0001-6889-7174","position":6,"is_corresponding":false},{"id":1356608,"name":"Visakuo Tsurho","orcid":null,"position":0,"is_corresponding":true}],"reference_count":32,"raw_metadata":null,"created_at":"2026-07-19T02:57:56.636458Z","pmid":"41038431","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}