{"doi":"10.1016/j.jmccpl.2025.100291","title":"Loss of Snord116 protects cardiomyocyte kinetics during ischemic stress","abstract":"Loss of Snord116, a non-coding RNA, causes Prader Willi Syndrome (PWS), a complex disorder with circadian, metabolic, neurologic, and cardiovascular phenotypes. The Snord116 paternal knockout (Snord116p-) mouse, a model of PWS, demonstrated differential methylation of thousands of genes involved in regulation of metabolism, epigenetics, and ion homeostasis. To determine if Snord116 expression influences the cardiomyocyte response to acute ischemia, we developed a model of ischemia and reperfusion using living myocardial slices and monitored cardiomyocyte function in slices derived from Snord116p- mice and wildtype littermates (WT LM) of both sexes. We found that Snord116 loss reduced ischemia-induced systolic prolongation and delayed diastolic elongation in slices from both males and females. Furthermore, when compared with slices from males, slices from females experienced a greater increase in end-diastolic force after ischemia. We conclude that female myocardium responds more dramatically and quickly to ischemic injury in this model and the lack of Snord116 is cardioprotective; this allows for a more complete myocardial recovery following reperfusion. • Using living myocardial slices from adult mice of both sexes, we developed a model of early cardiac ischemic injury with reperfusion. • Loss of Snord116, a non-coding RNA, reduced ischemia-induced systolic prolongation and delayed diastolic elongation in slices from both males and females. • Slices from females experienced a greater increase in end-diastolic force after ischemia relative to those from males. • Our results suggest inhibition of Snord116 protects contractile function and that females may experience greater deficit in cardiac function early during cardiac ischemia and reperfusion.","journal":"Journal of Molecular and Cellular Cardiology Plus","year":2025,"id":551869,"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":1,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9544,"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":740335,"name":"Emmaleigh N. Hancock","orcid":null,"position":1,"is_corresponding":false},{"id":1448145,"name":"Akshay Neeli","orcid":null,"position":2,"is_corresponding":false},{"id":1448146,"name":"Maria Sckolnick","orcid":null,"position":3,"is_corresponding":false},{"id":512922,"name":"Matthew A. Caporizzo","orcid":"0000-0002-9997-5718","position":4,"is_corresponding":false},{"id":369666,"name":"Bradley M. Palmer","orcid":"0000-0002-4388-3160","position":5,"is_corresponding":false},{"id":378039,"name":"Jeffrey L. Spees","orcid":"0000-0003-3560-3410","position":6,"is_corresponding":false},{"id":1448144,"name":"Lucy E. Pilcher","orcid":null,"position":0,"is_corresponding":true}],"reference_count":32,"raw_metadata":null,"created_at":"2026-07-19T02:54:29.318076Z","pmid":"40124788","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":[]}