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

Mitochondrial Membranes01:45

Mitochondrial Membranes

11.6K
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,...
11.6K
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

14.5K
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...
14.5K
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

16
Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
16
Mitochondrial Precursor Proteins01:39

Mitochondrial Precursor Proteins

2.6K
Mitochondrial precursors are partially unfolded or loosely folded polypeptide chains. Newly synthesized precursors are inhibited from spontaneously folding into their native conformation by the cytosolic chaperones, heat shock proteins 70 (Hsp70), and mitochondrial import stimulation factors (MSFs). Precursors bound to MSFs are guided to the TOM70-TOM37 receptors, while precursors bound to Hsp70  chaperones are targetted to TOM20-TOM22 receptor complexes.
Most of the mitochondrial...
2.6K
Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

3.2K
Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
3.2K
Mitochondria01:37

Mitochondria

13.8K
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,...
13.8K

You might also read

Related Articles

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

Sort by
Same author

Novel cardiovascular metabolic risk factor mechanisms and therapeutic opportunities.

European heart journal·2026
Same author

Telomer length, integrity vs. telomerase-activity: who is to blame for heart failure?

Cardiovascular research·2026
Same author

Cardiac mitochondrial proteome of lean, healthy Ossabaw minipigs with predisposition to metabolic syndrome versus that of Göttingen minipigs.

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

From bile to vessels: linking obesity to endothelial dysfunction.

European heart journal·2025
Same author

Angina with non-obstructive coronary arteries: haemodynamic phenotyping vs mechanistic pathophysiology.

European heart journal·2025
Same author

Importance of basic science and research training for the future generation of cardiologists.

European heart journal·2025
Same journal

Protection against postoperative atrial fibrillation via antiplatelet aggregation induced by remote ischemic preconditioning during off-pump coronary artery bypass grafting.

Basic research in cardiology·2026
Same journal

Peroxisomal catalase and plasmalogen biosynthesis protect from oxidative stress in Barth syndrome cardiomyopathy.

Basic research in cardiology·2026
Same journal

Bicuspid aortic valve stenosis is characterized by increased angiogenesis, inflammation, and a higher valvular-to-systemic calcification ratio than tricuspid aortic valve stenosis.

Basic research in cardiology·2026
Same journal

Myofilament-level effects of aficamten increase diastolic chamber volumes and maintain cardiac output through preserved length-dependent force generation in healthy rat and canine myocardium.

Basic research in cardiology·2026
Same journal

Functional rejuvenation of endothelial cell aging by transient reprogramming.

Basic research in cardiology·2026
Same journal

Coronary endothelial cells undergo venous-enriched disrupted maturation following myocardial infarction.

Basic research in cardiology·2026
See all related articles

Related Experiment Video

Updated: Jul 18, 2025

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

14.4K

Perspective: mitochondrial STAT3 in cardioprotection.

Petra Kleinbongard1

  • 1Institute for Pathophysiology, West German Heart and Vascular Center, University of Essen Medical School, Hufelandstr. 55, 45122, Essen, Germany. petra.kleinbongard@uk-essen.de.

Basic Research in Cardiology
|August 24, 2023
PubMed
Summary
This summary is machine-generated.

Signal transducer and activator of transcription 3 (STAT3) activation is crucial for heart protection during ischemia. Mitochondrial STAT3 enhances heart cell survival by improving mitochondrial function and reducing damage.

Keywords:
CardioprotectionIschemia/reperfusion injuryMitochondriaSAFE pathwaySTAT

More Related Videos

Subcellular Fractionation for ERK Activation Upon Mitochondrial-derived Peptide Treatment
07:55

Subcellular Fractionation for ERK Activation Upon Mitochondrial-derived Peptide Treatment

Published on: September 25, 2017

7.9K
Author Spotlight: Uncovering the Role of Mitochondrial Calcium Phosphate in Heart Failure and Bioenergetics
07:03

Author Spotlight: Uncovering the Role of Mitochondrial Calcium Phosphate in Heart Failure and Bioenergetics

Published on: August 23, 2024

865

Related Experiment Videos

Last Updated: Jul 18, 2025

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

14.4K
Subcellular Fractionation for ERK Activation Upon Mitochondrial-derived Peptide Treatment
07:55

Subcellular Fractionation for ERK Activation Upon Mitochondrial-derived Peptide Treatment

Published on: September 25, 2017

7.9K
Author Spotlight: Uncovering the Role of Mitochondrial Calcium Phosphate in Heart Failure and Bioenergetics
07:03

Author Spotlight: Uncovering the Role of Mitochondrial Calcium Phosphate in Heart Failure and Bioenergetics

Published on: August 23, 2024

865

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Cellular Signaling

Background:

  • Signal transducer and activator of transcription 3 (STAT3) is a critical signaling molecule in cardioprotection.
  • STAT3 activation is observed in both animal models and human studies related to heart protection.

Purpose of the Study:

  • To elucidate the role and mechanisms of STAT3 activation in cardioprotection.
  • To explore novel aspects of STAT3 involvement in heart protection, including genetic variations and therapeutic interventions.

Main Methods:

  • Investigated the canonical and non-canonical functions of STAT3 in response to ischemic conditioning.
  • Examined the localization and effects of activated STAT3 within mitochondria.
  • Discussed genetic variations and the impact of sodium-glucose cotransporter 2 inhibitors on STAT3 activation.

Main Results:

  • STAT3 activation upregulates cardioprotective and anti-apoptotic proteins.
  • Mitochondrial STAT3 enhances electron transport chain complex I activity, reduces reactive oxygen species, and prevents mitochondrial permeability transition pore opening.
  • Genetic variations in STAT may influence cardioprotection outcomes.

Conclusions:

  • STAT3 plays a multifaceted role in cardioprotection, acting both in the cytoplasm and mitochondria.
  • Mitochondrial STAT3 is a key mediator of cell survival during ischemic events.
  • STAT3 activation presents a potential therapeutic target for cardioprotection, possibly influenced by genetic factors and amenable to interventions like SGLT2 inhibitors.