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Related Experiment Video

Updated: Mar 10, 2026

Simultaneous Assessment of Cardiomyocyte DNA Synthesis and Ploidy: A Method to Assist Quantification of Cardiomyocyte Regeneration and Turnover
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YAP Induces a Prorenewal Metabolic State in Cardiomyocytes.

Lin Liu1, Jeffrey D Steimle2, Chang-Ru Tsai2

  • 1The McGill Gene Editing Laboratory (L.L., F.M., Y.Z., X.L., J.F.M.), The Texas Heart Institute at Baylor College of Medicine, Houston, TX.

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Summary

This study reveals that YAP reprogramming of cardiomyocyte metabolism can restore heart regeneration. By shifting mature cells to a neonatal-like state, YAP promotes cardiac repair after injury.

Keywords:
fatty acidsheart failuremyocardial infarctionmyocytes, cardiacphospholipids

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Area of Science:

  • Cardiovascular Biology
  • Molecular and Cellular Biology
  • Metabolic Regulation

Background:

  • Cardiomyocytes have limited renewal capacity, with regenerative potential decreasing after maturation.
  • Metabolic shifts from glycolysis to fatty acid oxidation during maturation create barriers to cardiomyocyte proliferation and cardiac repair.
  • The Hippo pathway effector YAP promotes cardiac regeneration, but its role in metabolic remodeling is unclear.

Purpose of the Study:

  • To investigate how YAP mediates metabolic remodeling in cardiomyocytes to overcome proliferation barriers.
  • To understand YAP's role in enabling cardiac regenerative repair after injury.
  • To explore YAP's impact on the balance between cardiomyocyte maturation and proliferation.

Main Methods:

  • Single-nucleus RNA sequencing and metabolomic analyses in mice to study YAP-induced metabolic remodeling.
  • Lipidomic analysis to assess YAP's impact on fatty acid catabolism and anabolism.
  • Assay for transposase-accessible chromatin with high-throughput sequencing (ATAC-seq), DNA footprinting, and RNA sequencing to identify YAP-regulated transcription factors.

Main Results:

  • YAP directs mature cardiomyocytes toward a neonatal-like metabolic state, reducing fatty acid utilization and promoting anabolism.
  • YAP inhibits the cardiac maturation transcription factor MEF2A, downregulating cardiomyocyte maturity pathways.
  • Perturbing MEF2A activity can interrupt maturation and restore cardiac regenerative capacity.

Conclusions:

  • YAP-mediated metabolic reprogramming is crucial for overcoming barriers to cardiomyocyte proliferation.
  • Targeting MEF2A offers a potential strategy to restore heart regeneration.
  • Understanding the interplay between metabolic maturation and proliferation provides insights for heart failure therapeutics.