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Related Experiment Video

Updated: Jul 26, 2025

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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TGF-β1/SMAD3 Regulates Programmed Cell Death 5 That Suppresses Cardiac Fibrosis Post-Myocardial Infarction by

Lin Weng1, Jingjing Ye2, Fenghe Yang1

  • 1Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, and State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China (L.W., F.Y., S.J., M.L., C.X., R.L., Y.X., Y. Zhou, J.Z., M.Z.).

Circulation Research
|June 22, 2023
PubMed
Summary
This summary is machine-generated.

Programmed cell death 5 (PDCD5) combats cardiac fibrosis by inhibiting histone deacetylase 3 (HDAC3). Upregulated PDCD5 ameliorates heart dysfunction and fibrosis, suggesting it as a therapeutic target.

Keywords:
cardiac dysfunctioncardiac fibrosisfibroblastsmyocardial infarctionnegative feedback factor

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Area of Science:

  • Cardiovascular Biology
  • Molecular Mechanisms of Disease
  • Fibrosis Research

Background:

  • Cardiac fibrosis contributes to heart failure, but its mechanisms are unclear.
  • Programmed cell death 5 (PDCD5) is expressed in the heart, yet its role in fibrosis is unknown.

Purpose of the Study:

  • To investigate the role and mechanisms of PDCD5 in cardiac fibrosis pathogenesis.
  • To explore PDCD5 as a potential therapeutic target for fibrotic heart disease.

Main Methods:

  • Measured PDCD5 levels in patients and mouse models of cardiac fibrosis.
  • Utilized cell culture and animal models to assess PDCD5 function in cardiac fibroblasts.
  • Investigated the interaction between PDCD5, SMAD3, and histone deacetylase 3 (HDAC3).

Main Results:

  • PDCD5 levels were elevated in fibrotic hearts and stimulated cardiac fibroblasts.
  • PDCD5 overexpression reduced fibrosis, while knockdown exacerbated it.
  • SMAD3 upregulates PDCD5, which inhibits HDAC3, thereby reducing fibrosis and improving cardiac function in mice.

Conclusions:

  • PDCD5 acts as a negative feedback regulator in cardiac fibrotic signaling.
  • PDCD5 ameliorates cardiac fibrosis and dysfunction by inhibiting HDAC3.
  • PDCD5 represents a promising therapeutic target for mitigating cardiac fibrosis progression.