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Updated: Jan 18, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

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PHGDH Orchestrates Cell Cycle Progression to Drive Cardiomyocyte Proliferation and Myocardial Regeneration via

Han Zhang1, Li Zhang1, Zehao Feng1

  • 1Department of Cardiology & Hongqiao International Institute of Medicine, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Cell Proliferation
|September 10, 2025
PubMed

Insights

Phosphoglycerate dehydrogenase (PHGDH) is vital for heart repair. Upregulating PHGDH promotes cardiomyocyte proliferation and myocardial regeneration, offering a new therapeutic target for heart damage.

Area of Science:

  • Cardiovascular Biology
  • Regenerative Medicine
  • Molecular Cardiology

Background:

  • The adult mammalian heart exhibits limited self-repair capabilities following injury.
  • Cardiomyocyte (CM) proliferation is crucial for cardiac regeneration, but it significantly declines after birth.
  • Identifying factors that promote CM proliferation is essential for developing cardiac repair strategies.

Purpose of the Study:

  • To investigate the role of phosphoglycerate dehydrogenase (PHGDH) in cardiomyocyte proliferation and myocardial regeneration.
  • To determine the therapeutic potential of modulating PHGDH activity for cardiac repair.

Main Methods:

  • Utilized mouse models of cardiac injury (apical resection and myocardial infarction).
  • Manipulated PHGDH expression (overexpression and inhibition with NCT-503) in vivo and in vitro.
  • Assessed cardiomyocyte proliferation, cardiac function, and underlying signaling pathways (cell cycle, TGF-β/Smad).

Main Results:

  • PHGDH expression diminishes during postnatal cardiac development.
  • PHGDH overexpression enhanced myocardial regeneration and cardiac function in mice after injury.
  • PHGDH inhibition abolished these regenerative effects.
  • PHGDH activation of the cell cycle and TGF-β/Smad signaling was observed.
  • PHGDH significantly promoted cardiac repair and CM proliferation in adult mice post-myocardial infarction.

Conclusions:

  • PHGDH is a key regulator of cardiomyocyte proliferation and myocardial regeneration.
  • Upregulating PHGDH offers a promising therapeutic strategy for promoting cardiac repair after heart damage.

Keywords:
PHGDHcardiomyocyte proliferationcell cyclemyocardial regeneration

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