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Related Concept Videos

Structure of Cardiac Muscles01:13

Structure of Cardiac Muscles

Cardiac muscle, or myocardium, is a specialized type of muscle found exclusively in the heart. Its unique structural and functional characteristics enable the heart to perform its vital role of pumping blood throughout the body continuously and rhythmically. The cardiac muscle cells, or cardiomyocytes, possess an endomysium and perimysium but do not have an epimysium.
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Specialized Characteristics of Cardiac Muscles01:27

Specialized Characteristics of Cardiac Muscles

The primary role of cardiac muscles is to propel blood throughout the cardiovascular system. The cardiac muscle cells, or cardiomyocytes, exhibit specialized characteristics that allow them to perform this function.
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Introduction to Fibroblasts01:09

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Smooth Muscle Contraction01:25

Smooth Muscle Contraction

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Isolation and Characterization of Adult Cardiac Fibroblasts and Myofibroblasts
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Published on: March 12, 2020

Myofibroblasts induce ectopic activity in cardiac tissue.

Michele Miragoli1, Nicolò Salvarani, Stephan Rohr

  • 1Department of Physiology, University of Bern, Bühlplatz 5, CH-3012 Bern, Switzerland.

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Myofibroblasts in heart tissue can trigger abnormal heart rhythms (tachyarrhythmias) by causing spontaneous electrical activity in cardiomyocytes. This interaction contributes to arrhythmias in conditions like heart attacks.

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Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
09:16

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

Published on: June 3, 2018

Area of Science:

  • Cardiovascular Biology
  • Cardiac Electrophysiology
  • Fibrosis Research

Background:

  • Focal ectopic activity in cardiac tissue initiates and sustains tachyarrhythmias.
  • Myofibroblasts in fibrotic hearts and scars depolarize cardiomyocytes via heterocellular electrotonic interactions.
  • This interaction occurs through gap junctions, potentially leading to abnormal automaticity.

Purpose of the Study:

  • To investigate if myofibroblast-cardiomyocyte interactions induce depolarization-induced abnormal automaticity.
  • To understand the role of myofibroblasts in cardiac arrhythmogenesis.
  • To elucidate the mechanism behind spontaneous activity in cardiomyocyte cultures.

Main Methods:

  • Cultured ventricular cardiomyocyte strands coated with myofibroblasts.
  • Density-dependent assessment of spontaneous activity.
  • Pharmacological (K(ATP) channel opener) and electrophysiological (current-clamp) analyses.
  • Experiments using connexin 43 transfected Hela cells versus wild-type Hela cells.

Main Results:

  • Myofibroblasts induced synchronized spontaneous activity in cardiomyocyte strands in a density-dependent manner.
  • Activity initiated at myofibroblast densities >15.7% and affected >80% of preparations at 50% density.
  • Spontaneous activity was confirmed as depolarization-induced automaticity, suppressed by K(ATP) channel opener and mimicked in single cardiomyocytes.
  • Functional gap junction communication (connexin 43) was necessary for the effect.

Conclusions:

  • Myofibroblast-cardiomyocyte interactions can induce abnormal automaticity and spontaneous activity.
  • This mechanism contributes to the spontaneous electromechanical activity observed in cardiomyocyte cultures.
  • Myofibroblasts in remodeled hearts may promote arrhythmogenesis by inducing ectopic activity.