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 Concept Videos

Electron Transport Chain: Complex I and II01:46

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...
Mitochondria01:37

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,...

You might also read

Related Articles

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

Sort by
Same author

Sulforaphane protects cardiomyoblasts against chemical hypoxia by increasing mitochondrial-ER communication and autophagy.

Chemico-biological interactions·2026
Same author

Mechanisms Involved in Pathological Succinate-Mediated Signaling.

International journal of molecular sciences·2026
Same author

Mitochondrial Dynamic Proteins MiD49 and MiD51 as Novel Targets of Cardioprotection.

Cells·2026
Same author

The Role of the Apelin Receptor in the Pathophysiology of Pulmonary Arterial Hypertension.

Cells·2026
Same author

Genomic Characterization of <i>Pseudomonas syringae</i> pv. <i>syringae</i> Populations Affecting Sweet Cherry Orchards in Chile Reveals Local Adaptation and Virulence Signatures.

Plants (Basel, Switzerland)·2026
Same author

Correction: IMproving Preclinical Assessment of Cardioprotective Therapies (IMPACT): a small animal acute myocardial infarction randomized-controlled multicenter study on the effect of ischemic preconditioning.

Basic research in cardiology·2025

Related Experiment Video

Updated: May 13, 2026

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
07:14

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation

Published on: July 13, 2018

Targeting mitochondria for cardiac protection.

Sauri Hernández-Reséndiz1, Mabel Buelna-Chontal, Francisco Correa

  • 1Department of Cardiovascular Biomedicine, National Institute of Cardiology Ignacio Chavez, Mexico City, Mexico.

Current Drug Targets
|March 6, 2013
PubMed
Summary

Mitochondria are vital for heart cell life and death. This review explores drugs targeting mitochondrial dysfunction in cardiovascular diseases, highlighting new therapeutic strategies.

More Related Videos

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
07:40

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy

Published on: May 26, 2023

Robust Mitochondrial Isolation from Rodent Cardiac Tissue
07:03

Robust Mitochondrial Isolation from Rodent Cardiac Tissue

Published on: August 23, 2024

Related Experiment Videos

Last Updated: May 13, 2026

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
07:14

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation

Published on: July 13, 2018

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
07:40

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy

Published on: May 26, 2023

Robust Mitochondrial Isolation from Rodent Cardiac Tissue
07:03

Robust Mitochondrial Isolation from Rodent Cardiac Tissue

Published on: August 23, 2024

Area of Science:

  • Cardiovascular Biology
  • Mitochondrial Medicine

Background:

  • Mitochondria are crucial for cardiomyocyte survival and death.
  • Mitochondrial dysfunction is implicated in various cardiac diseases.
  • Beyond energy production, mitochondria regulate calcium, reactive oxygen species (ROS), and protein modifications.

Purpose of the Study:

  • To review current drugs and compounds targeting mitochondria in cardiovascular diseases.
  • To highlight novel therapeutic strategies for cardiac conditions.

Main Methods:

  • Literature review of existing research on mitochondria and cardiovascular diseases.
  • Analysis of drugs and compounds targeting mitochondrial functions.
  • Synthesis of information on mitochondrial dynamics and protein modifications.

Main Results:

  • Mitochondrial dysfunction is a key factor in cardiac pathogenesis.
  • Emerging roles of mitochondrial fusion/fission and protein modifications (phosphorylation, nitrosylation) in heart disease.
  • Identification of various drugs and compounds under investigation for cardiovascular conditions.

Conclusions:

  • Targeting mitochondria offers promising therapeutic avenues for cardiovascular diseases.
  • Understanding mitochondrial dynamics and protein modifications is essential for developing new treatments.
  • Further research into mitochondrial-targeted therapies is warranted.