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

Mouse models of mitochondrial dysfunction and heart failure.

Laurie K Russell1, Brian N Finck, Daniel P Kelly

  • 1Center for Cardiovascular Research, Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8086, Saint Louis, MO 63110, USA.

Journal of Molecular and Cellular Cardiology
|December 30, 2004
PubMed
Summary

Mitochondrial metabolism is vital for heart function. Mouse models reveal how mitochondrial defects and fatty acid oxidation impact cardiomyopathy development and cardiac health.

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

Adipose Tissue Overexpression of Nicotinamide Phosphoribosyltransferase Prevents Metabolic Dysfunction in Obese Mice via Extracellular Vesicles.

Diabetes·2026
Same author

The Challenges and Promise of AI for Clinical Documentation in Pediatric Inpatient Care.

Hospital pediatrics·2026
Same author

Pharmacological rescue of mitochondrial dysfunction, neurite degeneration, and premature death of ALS and AD iPSC-derived neurons.

bioRxiv : the preprint server for biology·2026
Same author

The medium-chain fatty acid octanoate is a beneficial fuel for the failing heart.

American journal of physiology. Heart and circulatory physiology·2026
Same author

A Preoptic Neuronal Population Regulates Energy Expenditure and Balance.

bioRxiv : the preprint server for biology·2026
Same author

mTORC1 and nuclear ERK spatially control translation in cardiomyocytes through 4EBP1 phosphorylation.

Science signaling·2026

Area of Science:

  • Cardiovascular Biology
  • Mitochondrial Medicine
  • Metabolic Disorders

Background:

  • Mitochondria are crucial for energy production in the adult mammalian heart.
  • Oxidative metabolism in mitochondria is essential for maintaining proper cardiac function.
  • Mitochondrial dysfunction is implicated in various heart conditions, including cardiomyopathy.

Purpose of the Study:

  • To review mouse models that link mitochondrial metabolism to cardiac function.
  • To explore how manipulating mitochondrial energy pathways affects the heart.
  • To understand the role of mitochondrial defects in human cardiomyopathies.

Main Methods:

  • Utilizing gain- and loss-of-function mouse models.
  • Investigating alterations in mitochondrial energy transduction and ATP synthesis.

Related Experiment Videos

  • Examining pathways related to mitochondrial fatty acid oxidation.
  • Main Results:

    • Mouse models demonstrate the relevance of mitochondrial defects to human cardiomyopathies.
    • Chronic reliance on fatty acid oxidation, as seen in diabetic hearts, can lead to lipotoxicity and mitochondrial dysfunction.
    • These models help dissect the relationship between mitochondrial metabolism and cardiomyopathy.

    Conclusions:

    • Mitochondrial metabolism is a key determinant of cardiac function and disease.
    • Mouse models are invaluable tools for studying the molecular basis of mitochondrial cardiomyopathy.
    • Understanding these pathways can inform therapeutic strategies for heart failure and metabolic disorders.