<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Gomori K</submitter><funding>János Bolyai Re-search Fellowship of the Hungarian Academy of Sciences</funding><funding>Hungarian National Scientific Research Fund</funding><funding>NRDI Fund</funding><funding>EMBO short-term fellowship</funding><funding>New National Excellence Program</funding><funding>Eu-ropean HCEMM</funding><funding>EU's Horizon 2020</funding><funding>Thematic Excellence Programme</funding><funding>DFG (Deutsche Forschungsgemeinschaft)</funding><funding>Hungarian National Cardiovascular Laboratory</funding><pagination>2210</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9686542</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11(11)</volume><pubmed_abstract>Volume-induced hypertrophy is one of the risk factors for cardiac morbidity and mortality. In addition, mechanical and metabolic dysfunction, aging, and cellular redox balance are also contributing factors to the disease progression. In this study, we used volume overload (VO), which was induced by an aortocaval fistula in 2-month-old male Wistar rats, and sham-operated animals served as control. Functional parameters were measured by transthoracic echocardiography at termination 4- or 8-months after VO. The animals showed hypertrophic remodeling that was accompanied by mechanical dysfunction and increased cardiomyocyte stiffness. These alterations were reversible upon treatment with glutathione. Cardiomyocyte dysfunction was associated with elevated oxidative stress markers with unchanged</pubmed_abstract><journal>Antioxidants (Basel, Switzerland)</journal><pubmed_title>Altered Cellular Protein Quality Control System Modulates Cardiomyocyte Function in Volume Overload-Induced Hypertrophy.</pubmed_title><pmcid>PMC9686542</pmcid><funding_grant_id>8792</funding_grant_id><funding_grant_id>OTKA-138223, K139237</funding_grant_id><funding_grant_id>HU26307383</funding_grant_id><funding_grant_id>2019-1.1.1-PIACI-KFI-2019-00367</funding_grant_id><funding_grant_id>HA 7512/2-4 and HA 7512/2-1</funding_grant_id><funding_grant_id>UNKP-21-5-SZTE-543</funding_grant_id><funding_grant_id>No. 739593</funding_grant_id><funding_grant_id>RRF-2.3.1-21-2022-00003</funding_grant_id><funding_grant_id>2020-4.1.1.-TKP2020</funding_grant_id><funding_grant_id>bo_481_21</funding_grant_id><pubmed_authors>Ferdinandy P</pubmed_authors><pubmed_authors>Farkas-Morvay N</pubmed_authors><pubmed_authors>Begovic M</pubmed_authors><pubmed_authors>Budde H</pubmed_authors><pubmed_authors>Modi S</pubmed_authors><pubmed_authors>Kovacs A</pubmed_authors><pubmed_authors>Hassoun R</pubmed_authors><pubmed_authors>Pipis J</pubmed_authors><pubmed_authors>Lepran I</pubmed_authors><pubmed_authors>Mostafi N</pubmed_authors><pubmed_authors>Bencsik P</pubmed_authors><pubmed_authors>Gomori K</pubmed_authors><pubmed_authors>Delalat S</pubmed_authors><pubmed_authors>Gorbe A</pubmed_authors><pubmed_authors>Mugge A</pubmed_authors><pubmed_authors>Herwig M</pubmed_authors><pubmed_authors>Hamdani N</pubmed_authors><pubmed_authors>Szabados T</pubmed_authors></additional><is_claimable>false</is_claimable><name>Altered Cellular Protein Quality Control System Modulates Cardiomyocyte Function in Volume Overload-Induced Hypertrophy.</name><description>Volume-induced hypertrophy is one of the risk factors for cardiac morbidity and mortality. In addition, mechanical and metabolic dysfunction, aging, and cellular redox balance are also contributing factors to the disease progression. In this study, we used volume overload (VO), which was induced by an aortocaval fistula in 2-month-old male Wistar rats, and sham-operated animals served as control. Functional parameters were measured by transthoracic echocardiography at termination 4- or 8-months after VO. The animals showed hypertrophic remodeling that was accompanied by mechanical dysfunction and increased cardiomyocyte stiffness. These alterations were reversible upon treatment with glutathione. Cardiomyocyte dysfunction was associated with elevated oxidative stress markers with unchanged</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Nov</publication><modification>2025-04-19T16:13:21.383Z</modification><creation>2025-04-19T16:13:21.383Z</creation></dates><accession>S-EPMC9686542</accession><cross_references><pubmed>36358581</pubmed><doi>10.3390/antiox11112210</doi></cross_references></HashMap>