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Related Concept Videos

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Related Experiment Video

Updated: Sep 22, 2025

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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Fibroblasts Drive Metabolic Reprogramming in Pacemaker Cardiomyocytes.

Pei-Chun Chou1,2, Chih-Min Liu1,3, Ching-Hui Weng1,2

  • 1Division of Cardiology, Department of Medicine, Heart Rhythm Center (P.-C.C., C.-M.L., C.-H.W., J.-D.L., Y.-F.H.), Taipei Veterans General Hospital, Taiwan.

Circulation Research
|May 25, 2022
PubMed
Summary

Fibroblasts regulate heart rhythm by activating aerobic glycolysis in pacemaker cells through Aldoc. This interaction is crucial for sinoatrial node function and could lead to new therapies for rhythm failure.

Keywords:
fibroblastsglycolysisintegrinsmetabolomicsvertebrates

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Area of Science:

  • Cardiovascular Biology
  • Cellular Metabolism
  • Cardiac Electrophysiology

Background:

  • The sinoatrial node (SAN) microenvironment, comprising pacemaker cardiomyocytes (PCs) and fibroblasts, is vital for heart rhythm.
  • Altered SAN microenvironments can lead to cardiac rhythm failure.
  • Understanding fibroblast-PC interactions is key to elucidating SAN rhythm generation.

Purpose of the Study:

  • To investigate how fibroblasts interact with pacemaker cells and influence their metabolic reprogramming and rhythmic activity.
  • To identify the molecular mechanisms by which fibroblasts regulate the functional integrity of the SAN.

Main Methods:

  • Utilized Tbx18-induced PCs and fibroblasts for co-cultures and engineered tissues as in vitro models.
  • Employed RNA-sequencing, metabolomics, and cellular/molecular techniques.
  • Validated findings in vivo in rodents and human induced pluripotent stem cell-derived cardiomyocytes.

Main Results:

  • Fibroblasts activate aerobic glycolysis and metabolic reprogramming in PCs, regulating their rhythmicity.
  • This reprogramming is mediated by fibroblast-induced Aldoc (aldolase c) expression in PCs via an integrin-dependent signaling pathway.
  • Disruption of fibroblast-PC interaction or Aldoc knockdown abolished electrical activity; engineered tissues recapitulated SAN microenvironment function.

Conclusions:

  • Fibroblasts are critical regulators of SAN rhythmicity through Aldoc-mediated metabolic reprogramming.
  • This study reveals the cellular machinery underlying vertebrate SAN function.
  • Identifies a novel therapeutic target for cardiac rhythm disorders.