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Related Concept Videos

Development of the Heart01:27

Development of the Heart

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The development of the human heart, a crucial organ, commences from the mesoderm on the 18th or 19th day after fertilization. This process initiates in the cardiogenic area, a group of mesodermal cells at the embryo's head end, which evolves into elongated strands known as cardiogenic cords. These cords undergo a transformation to form hollow-centered endocardial tubes.
As the embryo undergoes lateral folding, these paired tubes approach each other, merging into a single primitive heart...
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ELABELA Targets Mitochondria to Modulate Heart Development.

Jian Wang1,2,3, Qingjie Wang1,2,3, Zhikang Xu1,2,3

  • 1Department of Pediatric Cardiology, Xinhua Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|April 7, 2026
PubMed
Summary
This summary is machine-generated.

Congenital heart disease (CHD) is linked to low levels of the peptide ELABELA (ELA). Restoring ELA levels in mice improved cardiac development, suggesting ELA as a potential biomarker and therapeutic target for fetal CHD.

Keywords:
BCL2/BAXELABELAcongenital heart diseasemitochondria

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Area of Science:

  • Cardiovascular Biology
  • Developmental Biology
  • Molecular Medicine

Background:

  • Congenital heart disease (CHD) is a major cause of infant mortality with unclear origins.
  • Current diagnostics and therapeutics for fetal CHD during pregnancy are limited.
  • Reliable biomarkers and treatment targets for fetal CHD are urgently needed.

Purpose of the Study:

  • To investigate the role of the endogenous peptide ELABELA (ELA) in the pathogenesis of fetal CHD.
  • To explore ELA as a potential biomarker for early detection of fetal CHD.
  • To evaluate ELA as a therapeutic target for preventing and managing fetal CHD.

Main Methods:

  • Analysis of ELA levels in human fetal cardiac tissues and plasma from pregnancies with and without CHD.
  • Utilizing mouse models with ELA deletion in cardiac progenitor cells to study its function.
  • Investigating the molecular mechanisms underlying ELA's role in cardiac development, including mitochondrial function and signaling pathways (APJ-AKT-BCL2/BAX).
  • Administering exogenous ELA to mouse models to assess its therapeutic potential.

Main Results:

  • Significantly reduced ELA levels were observed in human fetal cardiac tissues and plasma associated with CHD.
  • ELA deficiency in mice led to disrupted mitochondrial function and cardiac malformations.
  • ELA deficiency inhibited the APJ-AKT-BCL2/BAX pathway, causing mitochondrial swelling.
  • Exogenous ELA administration decreased CHD severity and incidence in mouse models.

Conclusions:

  • ELABELA (ELA) is a critical regulator of fetal cardiac development.
  • Reduced ELA levels are associated with human fetal CHD.
  • ELA shows promise as a diagnostic biomarker for fetal CHD.
  • ELA represents a potential therapeutic target for preventing and treating fetal CHD during gestation.