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The role of RORβ in human iPSC derived cardiomyocytes

dc.contributor.advisorHasenfuß, Gerd Prof. Dr.
dc.contributor.authorTorkieh, Setare
dc.date.accessioned2024-09-10T15:43:21Z
dc.date.available2024-10-08T00:50:10Z
dc.date.issued2024-09-10
dc.identifier.urihttp://resolver.sub.uni-goettingen.de/purl?ediss-11858/15476
dc.identifier.urihttp://dx.doi.org/10.53846/goediss-10727
dc.format.extent86de
dc.language.isoengde
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subject.ddc610de
dc.titleThe role of RORβ in human iPSC derived cardiomyocytesde
dc.typedoctoralThesisde
dc.contributor.refereeHasenfuß, Gerd Prof. Dr.
dc.date.examination2024-09-10de
dc.description.abstractengEvery year systolic heart failure contributes immensely to the death tolls in industrialized nations. However, little is known about the molecular mechanisms underlying this devastating disease. Based on the RNA sequencing screens of biopsies from aortic stenosis patients, RORβ is thought to play a role in the heart’s transition to failure. As a transcription factor its observed increase in expression, specifically during the state of compensated hypertrophy, might hint towards a relevant downstream effect. This thesis aims to provide a greater insight and understanding of the complex gene regulatory networks and molecular mechanisms underlying adaptive and adverse remodeling processes of the heart during its progression to failure. Thereby the focus lies on the role of RORβ during the CMs early stress response in regards of changes in cell viability and resilience. The outcomes of this study support the hypothesis that RORβ acts as a stress moderating factor on a transcriptional and functional level. This study identified RORβ as a novel actor during the hearts transition to failure. Transcriptional and functional analysis of AAV-RORβ transduced CMs have revealed its predicted role in upholding homeostatic processes. By reducing the impact of oxidative stress on the cell’s viability, it might allow for a state of compensated hypertrophy to be maintained and postpone the progression to failure. Further understanding of these molecular processes is crucial for future pharmacological research and the translational opportunity this thesis might offer in the establishment of druggable targets for the treatment of HF.de
dc.contributor.coRefereeZelarayan-Behrend, Laura Prof. Dr.
dc.subject.engHeart Failurede
dc.subject.engRetinoid acid related orphan-receptor betade
dc.subject.engCompensated Hypertophyde
dc.identifier.urnurn:nbn:de:gbv:7-ediss-15476-5
dc.affiliation.instituteMedizinische Fakultätde
dc.subject.gokfullInnere Medizin - Allgemein- und Gesamtdarstellungen (PPN619875747)de
dc.description.embargoed2024-10-08de
dc.identifier.ppn1902412362
dc.notes.confirmationsentConfirmation sent 2024-09-10T19:45:01de


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