{"doi":"10.1007/s12012-017-9412-4","title":"Exercise and Doxorubicin Treatment Modulate Cardiac Mitochondrial Quality Control Signaling","abstract":null,"journal":"Cardiovascular Toxicology","year":2018,"id":681586,"datarank":0.6190701577567639,"base_score":4.127134385045092,"endowment":4.127134385045092,"self_citation_contribution":0.6190701577567639,"citation_network_contribution":0.0,"self_endowment_contribution":0.6190701577567639,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":61,"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":1780808,"name":"E. Santos-Alves","orcid":null,"position":1,"is_corresponding":false},{"id":1780809,"name":"J. R. Torrella","orcid":null,"position":2,"is_corresponding":false},{"id":1780810,"name":"P. J. Oliveira","orcid":null,"position":3,"is_corresponding":false},{"id":1780811,"name":"J. Magalhães","orcid":null,"position":4,"is_corresponding":false},{"id":1780812,"name":"A. Ascensão","orcid":null,"position":5,"is_corresponding":false},{"id":1780806,"name":"I. Marques-Aleixo","orcid":"0000-0003-3438-0868","position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"Exercise and Doxorubicin Treatment Modulate Cardiac Mitochondrial Quality Control Signaling","abstract":"The cross-tolerance effect of exercise against heart mitochondrial-mediated quality control, remodeling and death-related mechanisms associated with sub-chronic Doxorubicin (DOX) treatment is yet unknown. We therefore analyzed the effects of two distinct chronic exercise models (endurance treadmill training-TM and voluntary free wheel activity-FW) performed during the course of the sub-chronic DOX treatment on mitochondrial susceptibility to permeability transition pore (mPTP), apoptotic and autophagic signaling and mitochondrial dynamics. Male Sprague-Dawley rats were divided into six groups (n = 6 per group): saline sedentary (SAL + SED), SAL + TM (12-weeks treadmill), SAL + FW (12-weeks voluntary free-wheel), DOX + SED [7-weeks sub-chronic DOX treatment (2 mg kg<sup>-1</sup> week<sup>-1</sup>)], DOX + TM and DOX + FW. Apoptotic signaling and mPTP regulation were followed by measuring caspase 3, 8 and 9 activities, Bax, Bcl2, CypD, ANT, and cophilin expression. Mitochondrial dynamics (Mfn1, Mfn2, OPA1 and DRP1) and auto(mito)phagy (LC3, Beclin1, Pink1, Parkin and p62)-related proteins were semi-quantified. DOX treatment results in augmented mPTP susceptibility and apoptotic signaling (caspases 3, 8 and 9 and Bax/Bcl2 ratio). Moreover, DOX decreased the expression of fusion-related proteins (Mfn1, Mfn2, OPA1), increased DRP1 and the activation of auto(mito)phagy signaling. TM and FW prevented DOX-increased mPTP susceptibility and apoptotic signaling, alterations in mitochondrial dynamics and inhibits DOX-induced increases in auto(mito)phagy signaling. Collectively, our results suggest that both used chronic exercise models performed before and during the course of sub-chronic DOX treatment limit cardiac mitochondrial-driven apoptotic signaling and regulate alterations in mitochondrial dynamics and auto(mito)phagy in DOX-treated animals.","is_dataset_classified":null,"base_score":0.0,"endowment":0.0,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"28536949","pmcid":null,"openalex_id":null,"authors":[],"funders":[{"funder_name":"Portuguese Foundation of Science and Technology","grant_id":"SFRH/BD/61889/2009","title":null},{"funder_name":"Portuguese Foundation of Science and Technology","grant_id":"SFRH/BPD/108322/2015","title":null},{"funder_name":"Portuguese Foundation of Science and Technology","grant_id":"SFRH/BD/112983/2015","title":null},{"funder_name":"Portuguese Foundation of Science and Technology","grant_id":"PTDC/DTP-DES/1071/2012","title":null},{"funder_name":"Portuguese Foundation of Science and Technology","grant_id":"PTDC/SAU-TOX/117912/2010","title":null},{"funder_name":"Portuguese Foundation of Science and Technology","grant_id":"Pest-C/SAU/LA0001/2013-2014","title":null},{"funder_name":"Portuguese Foundation of Science and Technology","grant_id":"UID/DTP/00617/2013","title":null}],"total_grants":7,"fwci":null,"citation_percentile":null,"influential_citations":0,"citation_trend":[],"oa_status":"closed","license":"http://www.springer.com/tdm","oa_locations":[{"url":"http://link.springer.com/article/10.1007/s12012-017-9412-4/fulltext.html","host_type":"publisher"},{"url":"http://link.springer.com/content/pdf/10.1007/s12012-017-9412-4.pdf","host_type":"publisher"}],"fields_of_study":[],"mesh_terms":["Mitochondria, Heart","Animals","Rats, Sprague-Dawley","Heart Diseases","Disease Models, Animal","Doxorubicin","Mitochondrial Proteins","Antibiotics, Antineoplastic","Exercise Therapy","Signal Transduction","Apoptosis","Mitochondrial Swelling","Physical Endurance","Running","Autophagy","Male","Apoptosis Regulatory Proteins","Mitochondrial Dynamics","Cardiotoxicity","Autophagy-Related Proteins","Mitophagy"],"keywords":["Heart mitochondria","adriamycin","Mitochondrial Quality Control","Chronic Exercise","Cardiac Cell Death"],"sdg_mappings":[],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[],"source":"live","citation_network_status":"fetched"},"created_at":"2026-08-17T18:11:44.996423Z","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":[]}