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

Ventricular remodeling: from bedside to molecule

R Jaffe1, M Y Flugelman, D A Halon

  • 1Department of Cardiology, Lady Davis Carmel Medical Center, Haifa, Israel.

Advances in Experimental Medicine and Biology
|January 1, 1997
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

Gender differences in the effects of cardiovascular drugs.

European heart journal. Cardiovascular pharmacotherapy·2017
Same author

Cardiovascular pharmacotherapy.

International journal of cardiology·2016
Same author

Co-expression of fibulin-5 and VEGF165 increases long-term patency of synthetic vascular grafts seeded with autologous endothelial cells.

Gene therapy·2015
Same author

Heart Failure, Saxagliptin, and Diabetes Mellitus: Observations from the SAVOR-TIMI 53 Randomized Trial.

Circulation·2015
Same author

Fibulin-5 regulates keloid-derived fibroblast-like cells through integrin beta-1.

International journal of cosmetic science·2015
Same author

The formation of an anti-restenotic/anti-thrombotic surface by immobilization of nitric oxide synthase on a metallic carrier.

Acta biomaterialia·2014
Same journal

Mammalian Respiratory Chain Complex Assemblies and Their Links to Mitochondria Stress-Induced Human Diseases.

Advances in experimental medicine and biology·2026
Same journal

Enzyme Assemblies in Nucleotide Metabolism: Structure, Regulation, and Disease Implications.

Advances in experimental medicine and biology·2026
Same journal

The Pyruvate Dehydrogenase Complex: A 90-Year-Old Enigma Shaping the Future of Structural Enzymology.

Advances in experimental medicine and biology·2026
Same journal

Regulation of the Anti-termination RNA Transcription Complex by Lon-Mediated Lambda N Degradation.

Advances in experimental medicine and biology·2026
Same journal

PCNA Macromolecular Complexes: PCNA Serves as a Molecular Hub Regulating Multiple Cellular Processes Inside and Outside of the Nucleus.

Advances in experimental medicine and biology·2026
Same journal

Dynamic Assemblies in Genome Maintenance.

Advances in experimental medicine and biology·2026
See all related articles

Heart failure results from maladaptive hypertrophy, cell death, and vascular changes, driven by complex molecular and genetic factors. Understanding these mechanisms is key to developing new treatments for ventricular remodeling.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Pathophysiology of Heart Failure

Background:

  • Myocardial remodeling is a complex process involving hypertrophy, ventricular dilatation, and heart failure.
  • The decompensation of hypertrophic remodeled myocardium involves synergistic mechanisms that are not fully understood.

Purpose of the Study:

  • To explore the molecular and genetic mechanisms underlying maladaptive hypertrophy and heart failure.
  • To identify key factors contributing to ventricular remodeling and decompensation.

Main Methods:

  • Analysis of myocardial gene expression.
  • Investigation of neurohormonal systems (e.g., renin-angiotensin).
  • Assessment of interstitial matrix composition and immune system components (e.g., TNF-alpha).

Related Experiment Videos

Main Results:

  • Maladaptive hypertrophy (abnormal myosin-actin production) contributes to progressive ventricular dilatation.
  • Programmed cell death (apoptosis) and changes in interstitial vasculature/collagen impact heart function.
  • Molecular factors include altered gene expression, activated neurohormonal systems, increased matrix metalloproteinase activity, and TNF-alpha expression.

Conclusions:

  • The decompensation of hypertrophic remodeled myocardium is multifactorial, involving maladaptive hypertrophy, apoptosis, and interstitial changes.
  • Understanding these molecular and genetic pathways is crucial for developing targeted therapies.
  • Future research aims to improve interventions for ventricular remodeling and heart failure.