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Updated: Jul 12, 2026
Ultrasonic Assessment of Myocardial Microstructure
Published on: January 14, 2014
The cardiac phospho-proteome during pressure overload in mice
Rhys Wardman1,2, Steve Grein1,2,3, Jennifer Schwartz4
1Department of Cardiovascular Physiology, European Center for Angioscience (ECAS), Medical Faculty Mannheim of Heidelberg University, Mannheim, Germany.
Insights
This study maps cardiac phosphoproteomic changes after transaortic constriction (TAC), revealing key alterations in hypertrophic signaling and metabolism. The findings offer insights into pressure overload heart failure and potential therapeutic targets.
Area of Science:
- Cardiovascular Biology
- Proteomics
- Molecular Cardiology
Background:
- Transaortic constriction (TAC) models pressure overload-induced cardiac hypertrophy and heart failure.
- Global cardiac phospho-proteome dynamics post-TAC are not fully understood.
Purpose of the Study:
- To characterize the cardiac phospho-proteomic signature at one and seven days after TAC.
- To identify altered phosphorylation events and cellular pathways involved in cardiac response to pressure overload.
Main Methods:
- Proteomic and phospho-proteomic analyses were performed on cardiac tissue post-TAC.
- Quantification of thousands of proteins and phosphorylation sites.
- Analysis of proteomic data from cardiomyocytes, endothelial cells, and fibroblasts.
Main Results:
- Hundreds of differential phosphorylation events were identified, significantly altered by pressure overload.
- Significant changes were observed in hypertrophic signaling, metabolic remodeling, contractile function, and stress response pathways.
- Cellular localization of phospho-proteins was determined, providing temporal and site-specific insights.
Conclusions:
- The study provides a comprehensive phospho-proteomic database of TAC-induced cardiac remodeling.
- Identified alterations offer potential novel therapeutic targets and biomarkers for heart failure.
- Publicly available data (PXD061784) facilitates further research into the molecular basis of cardiac remodeling.
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.
