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Related Experiment Video

Updated: May 5, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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ML216 Alleviates Age-Related Cardiac Fibrosis by Suppressing TGF-β1 Signaling Pathway.

Wenbin Liu1, Feng Cui1, Xiaodan Huang1

  • 1State Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences & School of Basic Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China.

International Journal of Molecular Sciences
|May 4, 2026
PubMed
Summary

Small molecule ML216 effectively reduces cardiac fibrosis by inhibiting transforming growth factor-β1 (TGF-β1) signaling. This compound shows promise for treating age-related heart conditions and preventing heart failure.

Keywords:
TGF-β1apoptosiscardiac agingfibrosis

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Area of Science:

  • Cardiovascular Biology
  • Pharmacology
  • Molecular Medicine

Background:

  • Cardiac fibrosis is a key factor in cardiac aging and heart failure development.
  • Current therapeutic options for cardiac fibrosis are limited.
  • Identifying novel therapeutic targets is crucial for managing fibrotic heart disease.

Purpose of the Study:

  • To investigate the antifibrotic effects of small-molecule compound ML216.
  • To elucidate the molecular mechanisms underlying ML216's action on cardiac fibrosis.
  • To evaluate ML216's therapeutic potential in aging-associated and induced cardiac fibrosis models.

Main Methods:

  • In vitro and in vivo studies using aging and isoproterenol-induced cardiac fibrosis models.
  • Assessment of transforming growth factor-β1 (TGF-β1) signaling pathway components.
  • Analysis of fibrotic gene expression (Col1a1, Cnn2, Acta2) and cardiomyocyte apoptosis.

Main Results:

  • ML216 significantly reduced cardiac fibrosis in both aging and induced models.
  • ML216 inhibited TGF-β1 signaling by decreasing TGF-β1 levels and SMAD phosphorylation.
  • ML216 suppressed downstream fibrotic markers (CTGF) and fibrotic genes, and reduced cardiomyocyte apoptosis.

Conclusions:

  • ML216 demonstrates potent antifibrotic effects by inhibiting the TGF-β1 pathway.
  • ML216 mitigates cardiac fibrosis by suppressing fibrotic signaling and cardiomyocyte apoptosis.
  • ML216 represents a promising therapeutic candidate for treating cardiac fibrosis and related heart conditions.