<div class="csl-bib-body">
<div class="csl-entry">Hofreither, D., Tomin, T., Jahnel, S., Mendjan, S., Schittmayer-Schantl, M., & Birner-Grünberger, R. (2023, May 12). <i>Proteomic and redox metabolomic investigation of pathological mechanisms of the failing heart</i> [Poster Presentation]. 30. Jahrestagung der AAS (Austrian Atherosclerosis Society), St. Gilgen, Austria. http://hdl.handle.net/20.500.12708/188019</div>
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dc.identifier.uri
http://hdl.handle.net/20.500.12708/188019
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dc.description.abstract
Oxidative stress plays a significant role in the development and progression of various pathologies. In heart failure, it is associated with multiple risk factors, such as diabetes and metabolic syndrome. Heart disease in different stages can further be linked to disrupted and abnormal metabolism in cardiac cells. To address the crosstalk of aberrant metabolism and alterations of the myocardial redox state correlated with oxidative stress and heart failure, differentially treated human stem cell-derived cardiac organoids (cardioids) were subjected to parallel mass spectrometry-based redox metabolomic and quantitative proteomic analyses. The impact of glucose availability and oxygen levels on the redox environment could be shown by the adaptive abundance of antioxidative enzymes specific to increased glycolytic flux or mitochondrial activity. Cardioids displayed distinct changes in the expression of proteins involved in collagen synthesis and modification, stress-mediated extracellular matrix remodelling, lipid metabolism and ion transport, as previously observed in the tissue of failing hearts. Additionally, metabolic alterations in response to hypoxic signalling further illustrate the impact of local oxygen concentrations on cellular activity. Results additionally disclosed the embryonic metabolic phenotype of the cardioid model, elucidating the importance of utilizing cardiac in vitro models appropriate to their respective translational ability to drive pathomolecular research. Alternatives were explored to address limitations. Ultimately, the design and implementation of a maturation media for AC16 proliferating human cardiomyocytes were carried out. RT-qPCR analysis revealed an improved phenotype as per the increased expression of multiple cardiomyocyte-specific markers.
en
dc.description.sponsorship
FWF Fonds zur Förderung der wissenschaftlichen Forschung (FWF)
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dc.language.iso
en
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dc.subject
redox stress
en
dc.subject
Heart failure
en
dc.subject
mass spectrometry
en
dc.title
Proteomic and redox metabolomic investigation of pathological mechanisms of the failing heart
en
dc.type
Presentation
en
dc.type
Vortrag
de
dc.contributor.affiliation
Austrian Academy of Sciences, Austria
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dc.contributor.affiliation
Austrian Academy of Sciences, Austria
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dc.relation.grantno
F 7309-B21
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dc.type.category
Poster Presentation
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tuw.project.title
Lipidhydrolyse im Krebs und in Lipid-assoziierten Krankheiten
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tuw.researchTopic.id
M6
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tuw.researchTopic.name
Biological and Bioactive Materials
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tuw.researchTopic.value
100
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tuw.publication.orgunit
E164-01-3 - Forschungsgruppe Bioanalytik
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tuw.publication.orgunit
E164-01 - Forschungsbereich Imaging und Instrumentelle Analytische Chemie
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tuw.author.orcid
0000-0002-7071-2316
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tuw.author.orcid
0000-0003-1147-9179
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tuw.author.orcid
0000-0001-7539-3951
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tuw.author.orcid
0000-0003-3950-0312
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tuw.event.name
30. Jahrestagung der AAS (Austrian Atherosclerosis Society)
en
tuw.event.startdate
12-05-2023
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tuw.event.enddate
13-05-2023
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tuw.event.online
On Site
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tuw.event.type
Event for scientific audience
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tuw.event.place
St. Gilgen
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tuw.event.country
AT
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tuw.event.presenter
Hofreither, Dominik
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tuw.event.track
Single Track
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wb.sciencebranch
Chemie
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wb.sciencebranch
Anatomie, Pathologie, Physiologie
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wb.sciencebranch.oefos
1040
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wb.sciencebranch.oefos
3011
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wb.sciencebranch.value
50
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wb.sciencebranch.value
50
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item.grantfulltext
none
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item.cerifentitytype
Publications
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item.fulltext
no Fulltext
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item.openairetype
conference poster not in proceedings
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item.openairecristype
http://purl.org/coar/resource_type/c_18co
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item.languageiso639-1
en
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crisitem.author.dept
E164-01-3 - Forschungsgruppe Bioanalytik
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crisitem.author.dept
E164-01-3 - Forschungsgruppe Bioanalytik
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crisitem.author.dept
Austrian Academy of Sciences
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crisitem.author.dept
Austrian Academy of Sciences
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crisitem.author.dept
E164-01-3 - Forschungsgruppe Bioanalytik
-
crisitem.author.dept
E164-01 - Forschungsbereich Imaging und Instrumentelle Analytische Chemie
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crisitem.author.orcid
0000-0002-7071-2316
-
crisitem.author.orcid
0000-0003-1147-9179
-
crisitem.author.orcid
0000-0001-7539-3951
-
crisitem.author.orcid
0000-0003-3249-655X
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crisitem.author.orcid
0000-0003-3950-0312
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crisitem.author.parentorg
E164-01 - Forschungsbereich Imaging und Instrumentelle Analytische Chemie
-
crisitem.author.parentorg
E164-01 - Forschungsbereich Imaging und Instrumentelle Analytische Chemie
-
crisitem.author.parentorg
E164-01 - Forschungsbereich Imaging und Instrumentelle Analytische Chemie
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crisitem.author.parentorg
E164 - Institut für Chemische Technologien und Analytik
