Jove
Visualize
Contact Us

Related Concept Videos

Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
Mitochondrial Membranes01:45

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,...
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...

You might also read

Related Articles

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

Sort by
Same author

The integrated stress response in apicomplexan and trypanosomatid parasites: balancing survival and pathogenesis.

Frontiers in immunology·2026
Same author

The integrated stress response suppresses PINK1-dependent mitophagy by preserving mitochondrial import efficiency.

Nature communications·2026
Same author

Myricetin mitigates trifloxystrobin neurotoxicity by modulating the integrated stress response pathway and antioxidant defense in sH-SY5Y cells.

Drug and chemical toxicology·2026
Same author

Trifloxystrobin induces oxidative stress-dependent activation of the OMA1-DELE1-HRI integrated stress response leading to apoptosis in human neuroblastoma cells.

Environmental pollution (Barking, Essex : 1987)·2025
Same author

Afucosylated IgG Promote Thrombosis in Mouse Injected with SARS-CoV-2 Spike Expressing Megakaryocytes.

International journal of molecular sciences·2025
Same author

FcRγIIA attenuates pathology of cutaneous leishmaniasis and modulates ITAMa/i balance.

Parasites & vectors·2024
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 Video

Updated: Jul 18, 2026

Isolation and Functional Analysis of Mitochondria from Cultured Cells and Mouse Tissue
09:27

Isolation and Functional Analysis of Mitochondria from Cultured Cells and Mouse Tissue

Published on: March 23, 2015

Mitochondrial fragmentation in apoptosis.

Damien Arnoult1

  • 1Unité de Physiopathologie des Infections Lentivirales, Institut Pasteur, 28 rue du Dr. Roux, 75724 Paris, cedex 15, France. damarn@pasteur.fr <damarn@pasteur.fr>

Trends in Cell Biology
|November 23, 2006
PubMed
Summary

Mitochondrial outer membrane permeabilization (MOMP) is a key step in apoptosis. This study concludes that mitochondrial fragmentation is not required for MOMP or cytochrome c release, challenging previous theories.

More Related Videos

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro
13:20

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro

Published on: July 17, 2018

A Faster, High Resolution, mtPA-GFP-based Mitochondrial Fusion Assay Acquiring Kinetic Data of Multiple Cells in Parallel Using Confocal Microscopy
10:45

A Faster, High Resolution, mtPA-GFP-based Mitochondrial Fusion Assay Acquiring Kinetic Data of Multiple Cells in Parallel Using Confocal Microscopy

Published on: July 20, 2012

Related Experiment Videos

Last Updated: Jul 18, 2026

Isolation and Functional Analysis of Mitochondria from Cultured Cells and Mouse Tissue
09:27

Isolation and Functional Analysis of Mitochondria from Cultured Cells and Mouse Tissue

Published on: March 23, 2015

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro
13:20

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro

Published on: July 17, 2018

A Faster, High Resolution, mtPA-GFP-based Mitochondrial Fusion Assay Acquiring Kinetic Data of Multiple Cells in Parallel Using Confocal Microscopy
10:45

A Faster, High Resolution, mtPA-GFP-based Mitochondrial Fusion Assay Acquiring Kinetic Data of Multiple Cells in Parallel Using Confocal Microscopy

Published on: July 20, 2012

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Mitochondrial outer membrane permeabilization (MOMP) is a critical event in apoptosis, leading to cytochrome c release and caspase activation.
  • Existing theories propose that MOMP is dependent on mitochondrial fission and fragmentation.
  • Conflicting evidence suggests mitochondrial fragmentation may occur after MOMP or even inhibit it under certain conditions.

Purpose of the Study:

  • To reconcile conflicting data regarding the role of mitochondrial fragmentation in MOMP.
  • To critically evaluate the necessity of mitochondrial fragmentation for MOMP and subsequent cytochrome c release.

Main Methods:

  • Literature review and critical analysis of existing studies on MOMP and mitochondrial dynamics.
  • Discussion of experimental evidence supporting and refuting the role of mitochondrial fragmentation in MOMP.

Main Results:

  • Evidence suggests that mitochondrial fragmentation is not consistently observed during MOMP.
  • In some experimental settings, mitochondrial fragmentation appears to occur subsequent to MOMP.
  • Data indicates that mitochondrial fragmentation can, in fact, inhibit MOMP under specific circumstances.

Conclusions:

  • Mitochondrial fragmentation is likely not a prerequisite for MOMP.
  • The release of cytochrome c into the cytosol can occur independently of mitochondrial fragmentation.
  • Re-evaluation of the molecular mechanisms underlying MOMP is warranted.