Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Infarct scar: a dynamic tissue.

Y Sun1, K T Weber

  • 1Division of Cardiovascular Diseases, Department of Internal Medicine, University of Tennessee, Memphis College of Medicine, Rm. 353 Dobbs Research Institute, 951 Court Avenue, Memphis, TN 38163, USA.

Cardiovascular Research
|April 25, 2000
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Exploratory study for identifying systemic biomarkers that correlate with pain response in patients with intervertebral disc disorders.

Immunologic research·2015
Same author

Recruitable ACE and tissue repair in the infarcted heart.

Journal of the renin-angiotensin-aldosterone system : JRAAS·2002
Same author

Aldosterone in congestive heart failure.

The New England journal of medicine·2002
Same author

Cardioreparation in hypertensive heart disease.

Hypertension (Dallas, Tex. : 1979)·2001
Same author

Renin expression at sites of repair in the infarcted rat heart.

Journal of molecular and cellular cardiology·2001
Same author

Fibrosis and hypertensive heart disease.

Current opinion in cardiology·2001
Same journal

Metabolic crisis and TRPM4 activation cause QT prolongation in TANGO2 deficiency disorder.

Cardiovascular research·2026
Same journal

Personalizing Atrial Fibrillation Therapy: Moving from Genetic Association to Mechanistic Translation.

Cardiovascular research·2026
Same journal

Placental Growth Factor Promotes Endothelial Activation and Inflammatory Remodelling in Pulmonary Hypertension.

Cardiovascular research·2026
Same journal

Endothelial-to-mesenchymal transition (EndMT) in atherosclerosis: mechanisms, models and therapies.

Cardiovascular research·2026
Same journal

The gut-heart axis in cardio-oncology.

Cardiovascular research·2026
Same journal

Proteomic signatures as biomarkers of atherosclerosis burden.

Cardiovascular research·2026
See all related articles

Myocardial infarction (MI) scar tissue is not inert but a dynamic, cellular component. This active infarct scar contributes to adverse cardiac remodeling and can be targeted by therapies.

Area of Science:

  • Cardiovascular Biology
  • Cardiac Pathophysiology
  • Tissue Engineering

Background:

  • Myocardial infarction (MI) scar was traditionally viewed as inert, acellular collagen tissue formed 6-8 weeks post-MI.
  • Recent molecular and cellular studies challenge this view, revealing scar complexity.

Purpose of the Study:

  • To investigate the dynamic nature of infarct scar tissue.
  • To explore the cellular composition, metabolic activity, and functional implications of cardiac scar post-MI.

Main Methods:

  • Utilized molecular and cellular biologic technologies to analyze infarct scar composition.
  • Investigated the presence of myofibroblasts (myoFb), neovasculature, and peptide generation components within the scar.

Main Results:

Related Experiment Videos

  • Infarct scar is cellular, containing myofibroblasts expressing alpha-smooth muscle actin (alpha-SMA).
  • Scar tissue is vascularized, metabolically active, and produces angiotensin peptides (Ang) and transforming growth factor (TGF)-beta1.
  • Scar contraction contributes to ventricular thinning and diastolic dysfunction; therapies targeting Angiotensin converting enzyme (ACE) or AT1 receptors attenuate scar activity.

Conclusions:

  • Infarct scar is a dynamic, contractile tissue, not inert filler.
  • Myofibroblasts and their associated molecular machinery drive scar remodeling and adverse cardiac changes.
  • Pharmacologic interventions targeting the renin-angiotensin system can modulate scar activity and mitigate negative remodeling.