# Notch signaling pathway and heart development, congenital heart disease, and myocardial regeneration

**Authors:** Yaping Liu, Xiaoxiao Wang, Xingyue Tao, Hao-Kun Zhang, Bingyan Liu, Yilin Li, Hang Wang, Huo-Min Luo, Hui-Lin Lv, Peifeng Li

PMC · DOI: 10.3389/fbioe.2025.1731605 · Frontiers in Bioengineering and Biotechnology · 2026-03-04

## TL;DR

This paper reviews how the Notch signaling pathway influences heart development, heart disease, and heart cell regeneration.

## Contribution

The paper provides a comprehensive review of Notch signaling's role in cardiac development and disease, highlighting its potential as a therapeutic target.

## Key findings

- Notch signaling regulates cardiac progenitor cell fate and heart morphogenesis.
- Dysregulation of Notch signaling is linked to congenital heart disease.
- Notch signaling influences cardiomyocyte proliferation and apoptosis.

## Abstract

This review summarizes the critical role of the Notch signaling pathway in cardiac development, congenital heart disease, and myocardial regeneration. The Notch signaling pathway exerts a profound impact on cardiac health and disease progression by finely regulating the fate determination of cardiac progenitor cells, cardiac morphogenesis, and the proliferation and apoptosis of cardiomyocytes. The article also explores the research progress of the Notch signaling pathway as a potential therapeutic target and looks forward to future research directions.

## Linked entities

- **Proteins:** Notch (neurogenic locus notch homolog)
- **Diseases:** congenital heart disease (MONDO:0005453)

## Full-text entities

- **Diseases:** congenital heart disease (MESH:D006330)

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12997049/full.md

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12997049/full.md

## References

101 references — full list in the complete paper: https://tomesphere.com/paper/PMC12997049/full.md

---
Source: https://tomesphere.com/paper/PMC12997049