The cardiac phospho-proteome during pressure overload in mice
Abstract Transaortic constriction (TAC) is a murine model of pressure overload-induced cardiac hypertrophy and heart failure. Despite its high prevalence during aortic stenosis or chronic arterial hypertension, the global alterations in cardiac phospho-proteome dynamics following TAC remain incomple...
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Nature Portfolio
2025-08-01
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| Series: | Scientific Data |
| Online Access: | https://doi.org/10.1038/s41597-025-05506-7 |
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| author | Rhys Wardman Steve Grein Jennifer Schwartz Frank Stein Joerg Heineke |
| author_facet | Rhys Wardman Steve Grein Jennifer Schwartz Frank Stein Joerg Heineke |
| author_sort | Rhys Wardman |
| collection | DOAJ |
| description | Abstract Transaortic constriction (TAC) is a murine model of pressure overload-induced cardiac hypertrophy and heart failure. Despite its high prevalence during aortic stenosis or chronic arterial hypertension, the global alterations in cardiac phospho-proteome dynamics following TAC remain incompletely characterised. We present a database of the phospho-proteomic signature one day and seven days after TAC. Utilising proteomic and phospho-proteomic analyses, we quantified thousands of proteins and phosphorylation sites, revealing hundreds of differential phosphorylation events significantly altered in the cardiac response to pressure overload. Our analysis highlights significant changes in hypertrophic signalling, metabolic remodelling, contractile function, and the stress response pathways. We present proteomic data from the main cardiac cell types (endothelial cells, fibroblasts and cardiomyocytes) to reveal the cellular localisation of the detected phospho-proteins, offering insights into temporal and site-specific phosphorylation events, facilitating the potential discovery of novel therapeutic targets and biomarkers. By making this resource publicly available (ProteomeXchange with identifier PXD061784) we aim to enable further exploration of the molecular basis of cardiac remodelling and advance translational research in heart failure. |
| format | Article |
| id | doaj-art-ec92ac03ed6f433db78e10801f4b640b |
| institution | Kabale University |
| issn | 2052-4463 |
| language | English |
| publishDate | 2025-08-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Scientific Data |
| spelling | doaj-art-ec92ac03ed6f433db78e10801f4b640b2025-08-20T03:42:23ZengNature PortfolioScientific Data2052-44632025-08-0112111210.1038/s41597-025-05506-7The cardiac phospho-proteome during pressure overload in miceRhys Wardman0Steve Grein1Jennifer Schwartz2Frank Stein3Joerg Heineke4Department of Cardiovascular Physiology, European Center for Angioscience (ECAS), Medical Faculty Mannheim of Heidelberg UniversityDepartment of Cardiovascular Physiology, European Center for Angioscience (ECAS), Medical Faculty Mannheim of Heidelberg UniversityProteomics Core Facility, European Molecular Biology Laboratory (EMBL)Proteomics Core Facility, European Molecular Biology Laboratory (EMBL)Department of Cardiovascular Physiology, European Center for Angioscience (ECAS), Medical Faculty Mannheim of Heidelberg UniversityAbstract Transaortic constriction (TAC) is a murine model of pressure overload-induced cardiac hypertrophy and heart failure. Despite its high prevalence during aortic stenosis or chronic arterial hypertension, the global alterations in cardiac phospho-proteome dynamics following TAC remain incompletely characterised. We present a database of the phospho-proteomic signature one day and seven days after TAC. Utilising proteomic and phospho-proteomic analyses, we quantified thousands of proteins and phosphorylation sites, revealing hundreds of differential phosphorylation events significantly altered in the cardiac response to pressure overload. Our analysis highlights significant changes in hypertrophic signalling, metabolic remodelling, contractile function, and the stress response pathways. We present proteomic data from the main cardiac cell types (endothelial cells, fibroblasts and cardiomyocytes) to reveal the cellular localisation of the detected phospho-proteins, offering insights into temporal and site-specific phosphorylation events, facilitating the potential discovery of novel therapeutic targets and biomarkers. By making this resource publicly available (ProteomeXchange with identifier PXD061784) we aim to enable further exploration of the molecular basis of cardiac remodelling and advance translational research in heart failure.https://doi.org/10.1038/s41597-025-05506-7 |
| spellingShingle | Rhys Wardman Steve Grein Jennifer Schwartz Frank Stein Joerg Heineke The cardiac phospho-proteome during pressure overload in mice Scientific Data |
| title | The cardiac phospho-proteome during pressure overload in mice |
| title_full | The cardiac phospho-proteome during pressure overload in mice |
| title_fullStr | The cardiac phospho-proteome during pressure overload in mice |
| title_full_unstemmed | The cardiac phospho-proteome during pressure overload in mice |
| title_short | The cardiac phospho-proteome during pressure overload in mice |
| title_sort | cardiac phospho proteome during pressure overload in mice |
| url | https://doi.org/10.1038/s41597-025-05506-7 |
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