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Updated: Jun 9, 2026
Generation and Expansion of Human Cardiomyocytes from Patient Peripheral Blood Mononuclear Cells
Published on: February 12, 2021
Activation of Notch signaling in cardiomyocytes during post-infarction remodeling
Erik Øie1, Wiggo J Sandberg, Mohammad Shakil Ahmed
1Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway. erik.oie@medisin.uio.no
Insights
The Notch signaling pathway is active in heart failure (HF) and plays a role in myocardial remodeling. This study found increased Notch3 and Notch4 signaling in cardiomyocytes during HF.
Area of Science:
- Cardiovascular Biology
- Molecular Signaling
- Cellular Remodeling
Background:
- Notch signaling is vital for cardiovascular development.
- Its role in myocardial remodeling during heart failure (HF) is not fully understood.
Purpose of the Study:
- To investigate Notch signaling activation in myocardial remodeling in heart failure (HF).
Main Methods:
- Examined Notch receptors and ligands in rat and human HF myocardial tissue.
- Assessed gene expression and protein localization.
- Analyzed isolated rat cardiomyocytes.
Main Results:
- Notch receptors, ligands, and NICD were present in myocardial tissue.
- Notch3 and Notch4 were identified as major receptors in cardiomyocytes.
- Upregulated Notch3 and Notch4 signaling was observed in chronic HF.
Conclusions:
- The Notch signaling system is present and activated in cardiomyocytes during HF.
- Notch signaling likely contributes to myocardial remodeling in heart failure.
Objective:
Notch signaling is crucial for cell-to-cell interaction during cardiovascular development and may influence differentiation, proliferation, and apoptotic events. We investigated whether Notch signaling is activated during myocardial remodeling in heart failure (HF).
Design:
Myocardial gene expression and localization of Notch receptors (Notch1-4) and ligands (Jagged1-2, and Delta-like (Dll)-1 and 4) were investigated in rats with HF after induction of myocardial infarction and in humans with HF.
Results:
All Notch receptors and ligands investigated and Notch intracellular domain (NICD) were present in rat and human myocardial tissue and in cardiomyocytes with differences in their relative expression levels and altered expression levels in failing vs. non-failing myocardium. In isolated rat cardiomyocytes, Notch3 and Notch4 appeared to be the major Notch receptors, and Notch3 and Notch4 mRNA levels and NICD-3 and -4 in cardiomyocytes were upregulated in chronic HF (p < 0.05), indicating increased Notch3 and Notch4 signaling.
Conclusion:
The Notch signaling system is present in the cardiomyocytes and activated in HF, indicating a role of Notch signaling during myocardial remodeling in HF.
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