{"doi":"10.1161/01.cir.90.2.653","title":"Ca(2+)-transporting ATPase, phospholamban, and calsequestrin levels in nonfailing and failing human myocardium.","abstract":"<jats:sec>\n            <jats:title>BACKGROUND</jats:title>\n            <jats:p>Observations of abnormalities in the diastolic components of intracellular Ca2+ transients in failing human left ventricular myocardium have raised the possibility that reductions in the level or function of sarcoplasmic reticulum proteins involved in Ca2+ transport contribute to the pathophysiology of dilated cardiomyopathy in humans. Functional assays, however, have revealed no differences in ATP-dependent Ca2+ transport or its modulation by phospholamban in sarcoplasmic reticulum-enriched microsomes prepared from nonfailing and failing human left ventricular myocardium. The purpose of the present study was to quantify protein levels of Ca(2+)-transporting ATPase, phospholamban, and calsequestrin directly in nonfailing and failing human left ventricular myocardium.</jats:p>\n          </jats:sec>\n          <jats:sec>\n            <jats:title>METHOD AND RESULTS</jats:title>\n            <jats:p>Total protein extracts were prepared from nonfailing left ventricular myocardium from the hearts of unmatched organ donors with normal left ventricular contractility (n = 6) and from failing left ventricular myocardium from the excised hearts of transplant recipients with class IV heart failure resulting from idiopathic dilated cardiomyopathy (n = 6). Ca(2+)-transporting ATPase, phospholamban, and calsequestrin contents were determined by quantitative immunoblotting with monoclonal and affinity-purified polyclonal antibodies. The levels of the three proteins were identical in nonfailing and failing human left ventricular myocardium.</jats:p>\n          </jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS</jats:title>\n            <jats:p>These results indicate that protein levels of Ca(2+)-transporting ATPase, phospholamban, and calsequestrin are not diminished in failing human left ventricular myocardium and that downregulation of the Ca(2+)-transporting ATPase and phospholamban is not part of the molecular pathophysiology of dilated cardiomyopathy in humans.</jats:p>\n          </jats:sec>","journal":"Circulation","year":1994,"id":670833,"datarank":12.614939864269154,"base_score":5.44673737166631,"endowment":5.44673737166631,"self_citation_contribution":0.8170106057499466,"citation_network_contribution":11.797929258519208,"self_endowment_contribution":0.8170106057499466,"citer_contribution":11.797929258519208,"corpus_percentile":null,"corpus_rank":null,"citation_count":231,"citer_count":200,"citers_with_citation_signal":189,"citers_with_endowment":189,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1752397,"name":"M Karimi","orcid":null,"position":1,"is_corresponding":false},{"id":1752398,"name":"K Green","orcid":null,"position":2,"is_corresponding":false},{"id":1752399,"name":"L R Jones","orcid":null,"position":3,"is_corresponding":false},{"id":1752396,"name":"M A Movsesian","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"Ca(2+)-transporting ATPase, phospholamban, and calsequestrin levels in nonfailing and failing human myocardium.","abstract":"<jats:sec>\n            <jats:title>BACKGROUND</jats:title>\n            <jats:p>Observations of abnormalities in the diastolic components of intracellular Ca2+ transients in failing human left ventricular myocardium have raised the possibility that reductions in the level or function of sarcoplasmic reticulum proteins involved in Ca2+ transport contribute to the pathophysiology of dilated cardiomyopathy in humans. Functional assays, however, have revealed no differences in ATP-dependent Ca2+ transport or its modulation by phospholamban in sarcoplasmic reticulum-enriched microsomes prepared from nonfailing and failing human left ventricular myocardium. The purpose of the present study was to quantify protein levels of Ca(2+)-transporting ATPase, phospholamban, and calsequestrin directly in nonfailing and failing human left ventricular myocardium.</jats:p>\n          </jats:sec>\n          <jats:sec>\n            <jats:title>METHOD AND RESULTS</jats:title>\n            <jats:p>Total protein extracts were prepared from nonfailing left ventricular myocardium from the hearts of unmatched organ donors with normal left ventricular contractility (n = 6) and from failing left ventricular myocardium from the excised hearts of transplant recipients with class IV heart failure resulting from idiopathic dilated cardiomyopathy (n = 6). Ca(2+)-transporting ATPase, phospholamban, and calsequestrin contents were determined by quantitative immunoblotting with monoclonal and affinity-purified polyclonal antibodies. The levels of the three proteins were identical in nonfailing and failing human left ventricular myocardium.</jats:p>\n          </jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS</jats:title>\n            <jats:p>These results indicate that protein levels of Ca(2+)-transporting ATPase, phospholamban, and calsequestrin are not diminished in failing human left ventricular myocardium and that downregulation of the Ca(2+)-transporting ATPase and phospholamban is not part of the molecular pathophysiology of dilated cardiomyopathy in humans.</jats:p>\n          </jats:sec>","is_dataset_classified":null,"base_score":5.44673737166631,"endowment":5.44673737166631,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"8044934","pmcid":null,"openalex_id":"https://openalex.org/W1980272147","authors":[],"funders":[{"funder_name":"NHLBI NIH HHS","grant_id":"HL-28556","title":null},{"funder_name":"NHLBI NIH HHS","grant_id":"HL-06308","title":null},{"funder_name":"NHLBI NIH HHS","grant_id":"HL-49428","title":null}],"total_grants":3,"fwci":10.1593,"citation_percentile":0.98656943,"influential_citations":0,"citation_trend":[{"year":2012,"count":3},{"year":2013,"count":3},{"year":2014,"count":4},{"year":2015,"count":3},{"year":2016,"count":2},{"year":2018,"count":2},{"year":2019,"count":1},{"year":2020,"count":4},{"year":2021,"count":2},{"year":2023,"count":1},{"year":2025,"count":1}],"oa_status":"bronze","license":null,"oa_locations":[{"url":"https://www.ahajournals.org/doi/pdf/10.1161/01.CIR.90.2.653","host_type":"journal"},{"url":"https://www.ahajournals.org/doi/pdf/10.1161/01.CIR.90.2.653","host_type":"publisher"},{"url":"https://doi.org/10.1161/01.cir.90.2.653","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/8044934","host_type":"repository"}],"fields_of_study":["Cardiac electrophysiology and arrhythmias","Viral Infections and Immunology Research","Cardiovascular Function and Risk Factors","Adenosine Triphosphatases","Adult","Calcium-Binding Proteins","Calcium-Transporting ATPases","Calsequestrin","Cardiomyopathy, Dilated","Down-Regulation","Humans","Immunoblotting","Middle Aged","Myocardium","Sarcoplasmic Reticulum","Ventricular Function, Left","Phospholamban"],"mesh_terms":["Phospholamban","Adenosine Triphosphatases","Calcium-Transporting ATPases","Adult","Calcium-Binding Proteins","Calsequestrin","Cardiomyopathy, Dilated","Humans","Middle Aged","Myocardium","Sarcoplasmic Reticulum","Immunoblotting","Down-Regulation","Ventricular Function, Left"],"keywords":["Phospholamban","Calsequestrin","Contractility","Internal medicine","Dilated cardiomyopathy","Medicine","Heart failure","Cardiomyopathy","Endoplasmic reticulum","Endocrinology","Diastole","Cardiology","Biology","Ryanodine receptor","Calcium","Biochemistry"],"sdg_mappings":[{"sdg_number":0,"sdg_label":"Good health and well-being"}],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[],"source":"live","citation_network_status":"fetched"},"created_at":"2026-08-16T00:09:37.039670Z","pmid":null,"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":[]}