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Updated: Jun 10, 2026

In vitro Assessment of Cardiac Reprogramming by Measuring Cardiac Specific Calcium Flux with a GCaMP3 Reporter
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Published on: February 22, 2022

Multi-Omics Integration Reveals Incomplete Reactivation of Developmental Cell-Cycle Programs in Adult Human Infarcted

Jieran Lyu1,2, Yuki Kuramoto1,3, Jun Li2,4

  • 1Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Osaka, Osaka, Japan.

Chemical Biology & Drug Design
|June 9, 2026
PubMed
Summary
This summary is machine-generated.

Adult heart regeneration is limited because cardiomyocytes fail to complete cell division. Key genes like ANLN and KIF18A are insufficient, but MDK shows promise for promoting cardiac repair.

Keywords:
acute myocardial infarctioncardiac regenerationcytokinesisgene regulatory network inferenceiPSC‐derived cardiomyocytesmulti‐omics integration

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Isolation, Culture and Transduction of Adult Mouse Cardiomyocytes
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Last Updated: Jun 10, 2026

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Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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Isolation, Culture and Transduction of Adult Mouse Cardiomyocytes
08:42

Isolation, Culture and Transduction of Adult Mouse Cardiomyocytes

Published on: August 28, 2016

Area of Science:

  • Cardiovascular Biology
  • Regenerative Medicine
  • Molecular Cardiology

Background:

  • Adult human hearts have minimal regenerative capacity post-myocardial infarction.
  • A small fraction of cardiomyocytes re-enter the cell cycle but fail to divide completely.

Purpose of the Study:

  • Investigate the molecular mechanisms preventing cardiomyocyte cell-cycle completion in adult hearts.
  • Identify potential therapeutic targets to enhance cardiac regeneration.

Main Methods:

  • Integrated multi-omics data (scRNA-seq, spatial transcriptomics, bulk RNA-seq, ATAC-seq) from fetal and adult human hearts.
  • Analyzed gene expression, chromatin accessibility, and regulatory networks.
  • Utilized human induced pluripotent stem cell-derived cardiomyocytes to test gene function under hypoxia and Wnt stimulation.

Main Results:

  • Cardiomyocytes in the infarct zone activated early cell-cycle programs but lacked late mitotic and cytokinesis machinery (e.g., ANLN, KIF18A).
  • Five key developmental cell-cycle genes (ANLN, KIF18A, MDK, RTKN2, SOX11) showed insufficient reactivation in adults.
  • MDK demonstrated responsiveness to pro-proliferative Wnt stimulation in cardiomyocytes, unlike other candidates under hypoxia.

Conclusions:

  • Incomplete cytokinesis reactivation is a major barrier to adult human cardiac regeneration.
  • MDK is a promising candidate for drug discovery to promote cardiomyocyte cell-cycle completion and cardiac repair.