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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.
Scientific Data
|August 2, 2025
Summary
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.
