{"doi":"10.1172/jci39434","title":"Cardiomyocyte PDGFR-β signaling is an essential component of the mouse cardiac response to load-induced stress","abstract":null,"journal":"Journal of Clinical Investigation","year":2010,"id":606721,"datarank":0.787053610824073,"base_score":5.247024072160486,"endowment":5.247024072160486,"self_citation_contribution":0.787053610824073,"citation_network_contribution":0.0,"self_endowment_contribution":0.787053610824073,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":189,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"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":716997,"name":"Di Ai","orcid":"0000-0003-2972-4582","position":1,"is_corresponding":false},{"id":1557658,"name":"Robert R. 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Understanding this effect of PDGFR inhibitors has been difficult because the role of PDGFR signaling in the heart remains largely unexplored. As described herein, we have found that PDGFR-beta expression and activation increase dramatically in the hearts of mice exposed to load-induced cardiac stress. In mice in which Pdgfrb was knocked out in the heart in development or in adulthood, exposure to load-induced stress resulted in cardiac dysfunction and heart failure. Mechanistically, we showed that cardiomyocyte PDGFR-beta signaling plays a vital role in stress-induced cardiac angiogenesis. Specifically, we demonstrated that cardiomyocyte PDGFR-beta was an essential upstream regulator of the stress-induced paracrine angiogenic capacity (the angiogenic potential) of cardiomyocytes. These results demonstrate that cardiomyocyte PDGFR-beta is a regulator of the compensatory cardiac response to pressure overload-induced stress. Furthermore, our findings may provide insights into the mechanism of cardiotoxicity due to anticancer PDGFR inhibitors.","is_dataset_classified":null,"base_score":5.247024072160486,"endowment":5.247024072160486,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"20071776","pmcid":"PMC2810076","openalex_id":"https://openalex.org/W2120608237","authors":[],"funders":[{"funder_name":"NIA NIH HHS","grant_id":"AG17899","title":null},{"funder_name":"NIA NIH HHS","grant_id":"R01 AG017899","title":null},{"funder_name":"NHLBI NIH HHS","grant_id":"R01 HL076661","title":null},{"funder_name":"NHLBI NIH HHS","grant_id":"HL076661","title":null},{"funder_name":"NHLBI NIH HHS","grant_id":"HL089792","title":null},{"funder_name":"NCRR NIH HHS","grant_id":"P41 RR011795","title":null},{"funder_name":"NHLBI NIH HHS","grant_id":"R01 HL089792","title":null},{"funder_name":"NHLBI NIH HHS","grant_id":"R01 HL022512","title":null},{"funder_name":"NIBIB NIH HHS","grant_id":"P41 EB002182","title":null},{"funder_name":"Howard Hughes Medical Institute","grant_id":"","title":null}],"total_grants":10,"fwci":10.6961,"citation_percentile":0.98729332,"influential_citations":0,"citation_trend":[{"year":2012,"count":23},{"year":2013,"count":15},{"year":2014,"count":15},{"year":2015,"count":12},{"year":2016,"count":17},{"year":2017,"count":16},{"year":2018,"count":13},{"year":2019,"count":9},{"year":2020,"count":8},{"year":2021,"count":11},{"year":2022,"count":9},{"year":2023,"count":8},{"year":2024,"count":7},{"year":2025,"count":4},{"year":2026,"count":5}],"oa_status":"bronze","license":null,"oa_locations":[{"url":"http://www.jci.org/articles/view/39434/files/pdf","host_type":"journal"},{"url":"http://www.jci.org/articles/view/39434/files/pdf","host_type":"publisher"},{"url":"https://doi.org/10.1172/jci39434","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/20071776","host_type":"repository"},{"url":"https://digitalcommons.library.tmc.edu/uthmed_docs/230","host_type":"repository"},{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/2810076","host_type":"repository"}],"fields_of_study":["Chemotherapy-induced cardiotoxicity and mitigation","Cancer, Hypoxia, and Metabolism","Neuroblastoma Research and Treatments"],"mesh_terms":["Animals","Body Weight","Coronary Circulation","Heart","Heart Failure","Mice, Inbred C57BL","Organ Size","Phosphorylation","Stroke Volume","Signal Transduction","Weight-Bearing","Mice, Knockout","Receptor, Platelet-Derived Growth Factor beta","Myocytes, Cardiac","Mice"],"keywords":["Heart failure","Regulator","Angiogenesis","Platelet-derived growth factor receptor","Cardiotoxicity","PDGFRB","Paracrine signalling","Biology","Medicine","Cancer research","Signal transduction","Pharmacology","Cell biology","Internal medicine","Receptor","Growth factor","Chemotherapy"],"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":"2026-07-30T05:04:01.482020Z","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":[]}