{"doi":"10.1371/journal.pone.0255452","title":"Polycystin-1 is required for insulin-like growth factor 1-induced cardiomyocyte hypertrophy","abstract":"Cardiac hypertrophy is the result of responses to various physiological or pathological stimuli. Recently, we showed that polycystin-1 participates in cardiomyocyte hypertrophy elicited by pressure overload and mechanical stress. Interestingly, polycystin-1 knockdown does not affect phenylephrine-induced cardiomyocyte hypertrophy, suggesting that the effects of polycystin-1 are stimulus-dependent. In this study, we aimed to identify the role of polycystin-1 in insulin-like growth factor-1 (IGF-1) signaling in cardiomyocytes. Polycystin-1 knockdown completely blunted IGF-1-induced cardiomyocyte hypertrophy. We then investigated the molecular mechanism underlying this result. We found that polycystin-1 silencing impaired the activation of the IGF-1 receptor, Akt, and ERK1/2 elicited by IGF-1. Remarkably, IGF-1-induced IGF-1 receptor, Akt, and ERK1/2 phosphorylations were restored when protein tyrosine phosphatase 1B was inhibited, suggesting that polycystin-1 knockdown deregulates this phosphatase in cardiomyocytes. Moreover, protein tyrosine phosphatase 1B inhibition also restored IGF-1-dependent cardiomyocyte hypertrophy in polycystin-1-deficient cells. Our findings provide the first evidence that polycystin-1 regulates IGF-1-induced cardiomyocyte hypertrophy through a mechanism involving protein tyrosine phosphatase 1B.","journal":"PLoS ONE","year":2021,"id":185510,"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":8,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9517,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2021-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":742052,"name":"Natalia Torrealba","orcid":"0000-0001-9321-4873","position":1,"is_corresponding":false},{"id":294623,"name":"Francisco Altamirano","orcid":"0000-0002-1612-2729","position":2,"is_corresponding":false},{"id":742053,"name":"Valeria Garrido‐Moreno","orcid":"0000-0002-3298-2622","position":3,"is_corresponding":false},{"id":737330,"name":"C. Vásquez","orcid":"0000-0003-2606-6860","position":4,"is_corresponding":false},{"id":742693,"name":"Raúl Flores-Vergara","orcid":null,"position":5,"is_corresponding":false},{"id":669161,"name":"Camila López‐Crisosto","orcid":"0000-0003-1055-099X","position":6,"is_corresponding":false},{"id":742054,"name":"María Paz Ocaranza","orcid":"0000-0002-4915-6378","position":7,"is_corresponding":false},{"id":632213,"name":"Mario Chiong","orcid":"0000-0002-5174-6545","position":8,"is_corresponding":false},{"id":742055,"name":"Zully Pedrozo","orcid":"0000-0003-4690-2803","position":9,"is_corresponding":false},{"id":251721,"name":"Sergio Lavandero","orcid":"0000-0003-4258-1483","position":10,"is_corresponding":false},{"id":742051,"name":"Carolina Fernández","orcid":"0009-0000-3017-5176","position":0,"is_corresponding":true}],"reference_count":46,"raw_metadata":null,"created_at":"2026-07-18T23:48:38.805613Z","pmid":"34407099","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":[]}