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Updated: Jul 6, 2025

Epigenetic Regulation of Cardiac Differentiation of Embryonic Stem Cells and Tissues
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Published on: June 3, 2016

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Cfp1 Controls Cardiomyocyte Maturation by Modifying Histone H3K4me3 of Structural, Metabolic, and Contractile Related

Changzhu Li1, Yang Zhang1, Jingling Shen2

  • 1Department of Pharmacology (State Key Laboratory of Frigid Zone Cardiovascular Disease, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang, 150086, P. R. China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|January 10, 2024
PubMed

Insights

CXXC zinc finger protein 1 (Cfp1) is crucial for cardiomyocyte maturation. Its deficiency impairs heart development and leads to cardiac disease, while its overexpression promotes maturation by regulating histone modifications.

Area of Science:

  • Epigenetics
  • Cardiovascular Biology
  • Developmental Biology

Background:

  • Cardiomyocyte maturation is essential for heart function, and its disruption causes severe cardiac diseases.
  • CXXC zinc finger protein 1 (Cfp1) is an epigenetic regulator with an underexplored role in heart development.
  • Understanding Cfp1's function is critical for addressing heart disease pathogenesis.

Purpose of the Study:

  • To investigate the role and underlying mechanisms of Cfp1 in cardiomyocyte maturation.
  • To determine the impact of Cfp1 deficiency and overexpression on cardiomyocyte development.
  • To elucidate Cfp1's epigenetic regulation of cardiac gene expression.

Main Methods:

  • Generation of cardiomyocyte-specific Cfp1 knockout (Cfp1-cKO) and transgenic (Cfp1-TG) mouse models.
  • Analysis of cardiomyocyte structure, metabolism, contractility, and cell cycle.
  • Utilized human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) for overexpression studies.
  • Assessed histone H3 lysine 4 trimethylation (H3K4me3) modifications and gene expression patterns.

Main Results:

  • Cfp1-cKO mice exhibited embryonic lethality within 4 weeks, with severely inhibited cardiomyocyte maturation.
  • Cfp1 deficiency led to structural, metabolic, contractile, and cell cycle abnormalities in cardiomyocytes.
  • Cfp1-TG mice and hiPSC-CMs overexpressing Cfp1 showed enhanced cardiomyocyte maturation.
  • Cfp1 regulates H3K4me3 modification, affecting the expression of fetal and adult cardiac genes.

Conclusions:

  • Cfp1 is a critical regulator of cardiomyocyte maturation, essential for normal heart development.
  • Dysfunction of Cfp1 is strongly linked to the pathogenesis of cardiac diseases.
  • Cfp1 modulates cardiomyocyte maturation through epigenetic control of key developmental genes via H3K4me3 modification.

Keywords:
Cfp1H3K4me3cardiomyocyte maturationhiPSC-CMs

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