Related Experiment Video

Updated: Jun 4, 2026

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
10:21

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix

Published on: June 14, 2016

Myocardial remodeling: cellular and extracellular events and targets

Jennifer A Dixon1, Francis G Spinale

  • 1Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston, 29425, USA.

Annual Review of Physiology
|February 15, 2011
PubMed

Insights

Stem cell treatments show promise in altering left ventricle remodeling after myocardial infarction (MI), even without long-term engraftment. Further research is needed to fully translate these findings into clinical practice.

Area of Science:

  • Cardiovascular Research
  • Regenerative Medicine
  • Translational Science

Background:

  • Left ventricle (LV) remodeling is a critical process following myocardial infarction (MI).
  • Cellular and extracellular pathways significantly influence post-MI LV remodeling.
  • Stem cell therapies are being investigated for their potential to modify this process.

Purpose of the Study:

  • To review translational studies on stem cell therapies for post-MI LV remodeling.
  • To explore the role of cellular and extracellular pathways in LV remodeling.
  • To investigate the mechanisms behind stem cell-mediated effects on LV remodeling.

Main Methods:

  • Analysis of large-animal models and clinical studies.
  • Examination of endogenous and exogenous stem cell effects.
  • Investigation of proteolytic pathways involved in post-MI remodeling.

Main Results:

  • Stem cell treatment can alter LV remodeling, irrespective of long-term cell engraftment.
  • A link exists between stem cell treatment post-MI and modulation of proteolytic pathways.
  • The full potential of stem cell treatments in clinical settings is yet to be achieved.

Conclusions:

  • Stem cells may exert beneficial effects on post-MI LV remodeling through an "echo effect."
  • Modulation of proteolytic pathways is a potential mechanism for stem cell efficacy.
  • Further translational research is crucial to optimize stem cell therapies for myocardial infarction recovery.

More Related Videos

Permanent Ligation of the Left Anterior Descending Coronary Artery in Mice: A Model of Post-myocardial Infarction Remodelling and Heart Failure09:37

Permanent Ligation of the Left Anterior Descending Coronary Artery in Mice: A Model of Post-myocardial Infarction Remodelling and Heart Failure

Published on: December 2, 2014

Related Concept Videos

Myocarditis I: Introduction01:21

Myocarditis I: Introduction

Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
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...
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...
Cellular Adaptation II: Hypertrophy01:26

Cellular Adaptation II: Hypertrophy

Hypertrophy is the increase in the size of individual cells, resulting in the enlargement of a tissue or organ. Unlike hyperplasia, which involves an increase in cell number, hypertrophy is characterized by an increase in cell volume. This process often occurs in response to higher functional demand or hormonal stimulation, leading to the production of more structural proteins and organelles, thereby enhancing the cells' work capacity.There are two primary types of hypertrophy: physiological...
Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
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...