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Related Experiment Video

Updated: Sep 3, 2025

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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Piezo1 Channel as a Potential Target for Hindering Cardiac Fibrotic Remodeling.

Nicoletta Braidotti1,2, Suet Nee Chen3, Carlin S Long4

  • 1Department of Physics, University of Trieste, Via A. Valerio 2, 34127 Trieste, Italy.

International Journal of Molecular Sciences
|July 28, 2022
PubMed
Summary

The mechanosensitive ion channel Piezo1, when upregulated after heart injury, drives cardiac fibrosis by promoting fibroblast activation and extracellular matrix production. Targeting Piezo1 may offer a novel therapeutic strategy for fibrotic diseases.

Keywords:
Piezo1cardiac remodelingcardiomyopathiesfibroblastsfibroblasts activationfibrosisheart diseasesmechanosensitive ion channelmyofibroblasts

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Area of Science:

  • Cardiovascular mechanobiology
  • Cellular mechanotransduction
  • Fibrosis research

Background:

  • Fibrotic tissues and neoplasms exhibit increased extracellular matrix (ECM) stiffness.
  • Mechanosensitive ion channels, like Piezo1, play roles in disease progression.
  • Cardiac fibrosis involves fibroblast activation and excessive ECM deposition.

Purpose of the Study:

  • To review the role of Piezo1 in disease, focusing on tumor progression and cardiac mechanobiology.
  • To explore Piezo1's involvement in cardiac fibrosis following myocardial injury.
  • To identify Piezo1 as a potential therapeutic target for fibrotic conditions.

Main Methods:

  • Review of recent scientific literature on Piezo1.
  • Analysis of Piezo1's role in fibroblast activation and ECM production.
  • Comparison of Piezo1's function in cardiac mechanobiology and cancer.

Main Results:

  • Piezo1 is upregulated in cardiac fibroblasts due to mechanical stress and inflammation post-myocardial injury.
  • Increased Piezo1 activity drives a positive feedback loop, exacerbating cardiac fibrosis.
  • Piezo1 mediates calcium influx, promoting cytoskeleton remodeling and myofibroblast differentiation.

Conclusions:

  • Piezo1 activation contributes to fibroblast activation, myofibroblast recruitment, and excessive ECM production in cardiac fibrosis.
  • Targeting Piezo1 presents a potential therapeutic avenue for mitigating fibrotic progression.
  • Understanding Piezo1's role offers new insights into treating fibrotic diseases, including cardiac fibrosis.