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

Necrosis01:16

Necrosis

4.7K
Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
4.7K
Mitochondrial Membranes01:45

Mitochondrial Membranes

11.8K
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,...
11.8K
Mitochondrial Protein Sorting01:39

Mitochondrial Protein Sorting

4.4K
Mitochondria are double-membrane organelles of the eukaryotes involved in cellular metabolism, signaling, ATP synthesis, and programmed cell death.  Each of these processes requires specific proteins and enzymes that must be correctly sorted to the right mitochondrial subcompartment for the proper functioning of the organelle.
Most of these mitochondrial proteins are encoded by the nucleus and imported to the mitochondria as unfolded or loosely folded precursors. Mitochondrial precursors...
4.4K
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
Protein Transport into the Inner Mitochondrial Membrane01:34

Protein Transport into the Inner Mitochondrial Membrane

4.0K
Nuclear encoded mitochondrial precursors are imported to the inner membrane in a multistep process involving two separate translocons, TIM22 and TIM23. TIM23 is a cation-selective pore that remains closed by the N terminal segment of the protein. Negative charges on the TIM23 act as a receptor for the incoming precursor, pulling the positively charged matrix-targeting sequence for peptide insertion and translocation.
Transport of mitochondrial precursors across the TIM23 channel is driven by...
4.0K
The Inner Mitochondrial Membrane01:28

The Inner Mitochondrial Membrane

3.5K
The inner mitochondrial membrane is the primary site of ATP synthesis. The inner membrane domain that forms a smooth layer adjacent to the outer membrane is called the inner boundary membrane. This domain contains membrane transporters that drive metabolites in and out of the mitochondria.  In contrast, the inner membrane network that invaginates into the matrix space is called the cristae membrane. This domain accounts for principle mitochondrial function as it accommodates the protein...
3.5K

You might also read

Related Articles

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

Sort by
Same author

Mutation of a single cysteine in CaMKIIδ protects the heart from ischemia-reperfusion Injury.

bioRxiv : the preprint server for biology·2026
Same author

Severe obesity in human HFpEF alters contractile protein function and organization.

Science (New York, N.Y.)·2026
Same author

Loss of TMEM65 in mice causes mitochondrial disease mediated by mitochondrial Ca<sup>2</sup>.

Nature communications·2026
Same author

Organ preservation with total neoadjuvant therapy in early-stage rectal cancer: A statewide analysis.

Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland·2026
Same author

Protean Manifestations of Systemic Lupus Erythematosus With Antiphospholipid Syndrome: A Case Report of a Rare Variant of Libman-Sack's Endocarditis and Optic Perineuritis.

ACR open rheumatology·2026
Same author

A Review of Well-being Assessment Instruments in Hospital Medicine.

Journal of general internal medicine·2026

Related Experiment Video

Updated: Aug 20, 2025

Assessment of Open Probability of the Mitochondrial Permeability Transition Pore in the Setting of Coenzyme Q Excess
07:35

Assessment of Open Probability of the Mitochondrial Permeability Transition Pore in the Setting of Coenzyme Q Excess

Published on: June 1, 2022

2.3K

Mitochondrial permeability transition pore-dependent necrosis.

Dexter J Robichaux1, Mikako Harata2, Elizabeth Murphy2

  • 1Department of Integrative Physiology, Baylor College of Medicine, Houston, TX, USA; Cardiovascular Research Institute, Baylor College of Medicine, Houston, TX, USA.

Journal of Molecular and Cellular Cardiology
|November 21, 2022
PubMed
Summary

Mitochondrial permeability transition pore (mPTP)-dependent cell death involves mitochondrial dysfunction and is linked to heart and brain injuries. Targeting the mPTP may reduce tissue damage after ischemic events.

Keywords:
ANTATP synthaseBAKBAXCalciumCypDIschemia reperfusionMPTPMitochondriaMitochondrial dysfunctionNecrosisPermeability transitionROS

More Related Videos

Multi-parameter Measurement of the Permeability Transition Pore Opening in Isolated Mouse Heart Mitochondria
13:42

Multi-parameter Measurement of the Permeability Transition Pore Opening in Isolated Mouse Heart Mitochondria

Published on: September 7, 2012

21.6K
Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis
08:55

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Published on: August 7, 2018

10.9K

Related Experiment Videos

Last Updated: Aug 20, 2025

Assessment of Open Probability of the Mitochondrial Permeability Transition Pore in the Setting of Coenzyme Q Excess
07:35

Assessment of Open Probability of the Mitochondrial Permeability Transition Pore in the Setting of Coenzyme Q Excess

Published on: June 1, 2022

2.3K
Multi-parameter Measurement of the Permeability Transition Pore Opening in Isolated Mouse Heart Mitochondria
13:42

Multi-parameter Measurement of the Permeability Transition Pore Opening in Isolated Mouse Heart Mitochondria

Published on: September 7, 2012

21.6K
Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis
08:55

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Published on: August 7, 2018

10.9K

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pathology

Background:

  • Mitochondrial permeability transition pore (mPTP)-dependent cell death is a necrotic process.
  • It is triggered by mitochondrial dysfunction, elevated Ca2+ and reactive oxygen species.
  • This cell death pathway is implicated in ischemic injuries and degenerative diseases.

Purpose of the Study:

  • To review molecular triggers and regulators of mPTP-dependent necrosis.
  • Focus on myocardial ischemia reperfusion injury.
  • Discuss downstream consequences and future research directions.

Main Methods:

  • Literature review of research over the past 50 years.
  • Identification of mPTP regulators and pore-forming components.
  • Analysis of downstream effects and therapeutic potential.

Main Results:

  • Significant progress in identifying mPTP regulators and components.
  • Understanding of molecular triggers and consequences of mPTP opening.
  • Potential therapeutic strategies targeting mPTP are emerging.

Conclusions:

  • mPTP-dependent cell death is a key mechanism in ischemic injury.
  • Targeting the mPTP offers a promising therapeutic avenue.
  • Further research is needed to fully elucidate mPTP function and therapeutic applications.