Related Experiment Video

Updated: Mar 25, 2026

Pluripotent Stem Cell Derived Cardiac Cells for Myocardial Repair
06:37

Pluripotent Stem Cell Derived Cardiac Cells for Myocardial Repair

Published on: February 3, 2017

8.9K

Atrophied cardiomyocytes and their potential for rescue and recovery of ventricular function

Mark R Heckle1, David M Flatt2, Yao Sun2

  • 1Department of Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.

Heart Failure Reviews
|February 14, 2016
PubMed

Insights

Atrophic cardiomyocytes in fibrotic hearts can be rescued. This process involves understanding how angiotensin II and low triiodothyronine (T3) signaling contribute to myocyte atrophy, offering a complementary approach to cardiac regeneration.

Area of Science:

  • Cardiovascular Biology
  • Cellular Physiology
  • Cardiac Pathophysiology

Background:

  • Myocyte size is workload-dependent, with both hypertrophy and atrophy observed in the heart.
  • Myocyte atrophy occurs with fibrosis, often due to immobilization and protein degradation via the ubiquitin-proteasome system.
  • Atrophy also involves dedifferentiation and re-expression of fetal genes, influenced by low intracellular triiodothyronine (T3).

Purpose of the Study:

  • To elucidate the mechanisms of myocyte atrophy in fibrotic heart tissue.
  • To identify the role of heterocellular signaling and specific molecular pathways in inducing myocyte atrophy.
  • To explore the potential for rescuing atrophic myocytes to improve cardiac function.

Main Methods:

  • Investigated mechanisms of myocyte immobilization and protein degradation.
  • Analyzed the role of low intracellular T3 and thyroid hormone receptor β1 in myocyte dedifferentiation.
  • Examined heterocellular signaling between myofibroblasts and myocytes, focusing on angiotensin II and its effects on calcium and T3 levels.

Main Results:

  • Myocyte atrophy is linked to immobilization, ubiquitin-proteasome system activity, and dedifferentiation.
  • Scar myofibroblasts generate angiotensin II, inducing paracrine signaling that leads to myocyte calcium overload and oxidative stress.
  • Oxidative stress activates deiodinase-3, degrading T3 and creating a low T3 state that promotes atrophy.
  • Atrophic myocytes were identified as a viable population within the failing heart.

Conclusions:

  • Atrophic myocytes in fibrotic hearts result from a complex interplay of mechanical stress, signaling pathways (angiotensin II), and altered thyroid hormone metabolism.
  • These atrophic myocytes represent a potentially salvageable pool of cells that could be therapeutically targeted.
  • Myocyte rescue offers a complementary strategy to progenitor cell-based therapies for myocardial regeneration and functional recovery.

Keywords:
Angiotensin IIDeiodinase-3Low intracellular T3Myocyte atrophyOxidative stressRebuilding myocardiumUbiquitin ligases

More Related Videos

Isolation and Functional Characterization of Human Ventricular Cardiomyocytes from Fresh Surgical Samples14:39

Isolation and Functional Characterization of Human Ventricular Cardiomyocytes from Fresh Surgical Samples

Published on: April 21, 2014

18.0K
In Vitro Differentiation of Human Mesenchymal Stem Cells into Functional Cardiomyocyte-like Cells09:05

In Vitro Differentiation of Human Mesenchymal Stem Cells into Functional Cardiomyocyte-like Cells

Published on: August 9, 2017

11.5K

Related Concept Videos

Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...
743
Cardiomyopathy V: Interprofessional Care01:29

Cardiomyopathy V: Interprofessional Care

Managing cardiomyopathy involves addressing underlying or precipitating causes, treating heart failure with medications, and implementing dietary changes and a balanced exercise and rest regimen.Lifestyle ModificationsCardiomyopathy patients should adopt a low-sodium diet to reduce fluid retention and manage heart failure. A personalized exercise and rest plan helps maintain physical fitness without overstraining the heart. Avoiding alcohol and tobacco is essential to prevent further damage to...
621
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
1.3K
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
671