Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Mitochondria

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...

Electron Transport Chain: Complex I and II

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...

Pathophysiology of Heart Failure

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...

The Supercomplexes in the Crista Membrane

The Supercomplexes in the Crista Membrane

The mitochondrial cristae membrane is the primary site for the oxidative phosphorylation (OXPHOS) process of energy conversion mediated through respiratory complexes I to V. These complexes have been widely studied for decades, and it has been proven that they form supramolecular structures called respiratory supercomplexes (SC). These higher-order complexes may be crucial in maintaining the biochemical structure and improving the physiological activity of the individual complexes while...

Heart Failure I: Introduction

Heart Failure I: Introduction

Heart failure refers to a clinical syndrome caused by structural or functional cardiac disorders that prevent the heart from pumping an adequate amount of blood to meet the body's metabolic needs. This condition often arises from myocardial infarction or ischemia, leading to decreased cardiac output, reduced tissue perfusion, impaired gas exchange, fluid volume imbalance, and decreased functional ability.Heart failure can result from disruptions in the mechanisms that regulate cardiac output...

Mitochondrial Membranes

Mitochondrial Membranes

A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...

You might also read

Related Articles

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

Sort by

Same author

Oxygen Transport Impairment in the Failing Heart: A Histology-Image-Based Computational Analysis.

Annals of biomedical engineering·2026

Same author

Dietary Protein Restriction Ameliorates Cardiac Inflammaging via AMPK-ULK1-Mediated Mitochondrial Quality Control.

Aging cell·2026

Same author

Improving 24-Hour Medication Reconciliation Through Audit and Feedback: A Multicycle Quality Improvement Study at a Scottish District General Hospital.

Cureus·2025

Same author

Novel insights into beta cell ER stress CHOP and its role in HFpEF development.

Cardiovascular diabetology·2025

Same author

Evidence of Hyperacetylation of Mitochondrial Regulatory Proteins in Left Ventricular Myocardium of Dogs with Chronic Heart Failure.

International journal of molecular sciences·2025

Same author

Contemporary insights into elamipretide's mitochondrial mechanism of action and therapeutic effects.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie·2025

Search research articles

Related Experiment Video

Updated: Jul 2, 2026

Robust Mitochondrial Isolation from Rodent Cardiac Tissue

Robust Mitochondrial Isolation from Rodent Cardiac Tissue

Published on: August 23, 2024

Cardiac mitochondria in heart failure: decrease in respirasomes and oxidative phosphorylation.

Mariana G Rosca¹, Edwin J Vazquez, Janos Kerner

¹Department of Medicine, School of Medicine, Case Western Reserve University, 10900 Euclid Avenue, Cleveland 44106-4981, OH, USA.

Cardiovascular Research

|August 20, 2008

Summary

This summary is machine-generated.

Heart failure involves mitochondrial dysfunction. In a canine model, we found that the electron transport chain (ETC) supercomplex assembly, not individual components, was defective, impairing oxidative phosphorylation.

More Related Videos

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

Published on: January 19, 2017

Respirometric Oxidative Phosphorylation Assessment in Saponin-permeabilized Cardiac Fibers

Respirometric Oxidative Phosphorylation Assessment in Saponin-permeabilized Cardiac Fibers

Published on: February 28, 2011

Related Experiment Videos

Last Updated: Jul 2, 2026

Robust Mitochondrial Isolation from Rodent Cardiac Tissue

Robust Mitochondrial Isolation from Rodent Cardiac Tissue

Published on: August 23, 2024

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

Published on: January 19, 2017

Respirometric Oxidative Phosphorylation Assessment in Saponin-permeabilized Cardiac Fibers

Respirometric Oxidative Phosphorylation Assessment in Saponin-permeabilized Cardiac Fibers

Published on: February 28, 2011

Area of Science:

Biochemistry
Cardiology
Mitochondrial Biology

Background:

Mitochondrial dysfunction is a key factor in heart failure (HF).
Existing research shows variable electron transport chain (ETC) defects in cardiomyopathies.
A consistent trend for ETC defects in HF is not well-defined.

Purpose of the Study:

To define the defect in cardiac mitochondrial integrative function in a model of heart failure induced by coronary microembolization.
To investigate the role of ETC supercomplex assembly in heart failure.

Main Methods:

Utilized a canine model of coronary microembolization-induced heart failure.
Assessed oxidative phosphorylation using various substrates to evaluate mitochondrial membrane transport, dehydrogenase activity, and electron transport coupled to ATP synthesis.
Investigated ETC supramolecular organization using native gel electrophoresis.

Main Results:

Observed a significant decrease in ADP-stimulated respiration, unaffected by uncouplers.
Found a normal ADP/O ratio, indicating intact phosphorylation apparatus.
Identified normal individual ETC complex activities but a decreased amount of the essential ETC supercomplex (respirasome).

Conclusions:

The primary mitochondrial defect in this heart failure model is in the supermolecular assembly of the ETC.
This defect in ETC supercomplexes, rather than individual components, impairs oxidative phosphorylation and contributes to heart failure.