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 Experiment Videos

Preconditioning delays Ca2+-induced mitochondrial permeability transition.

Laurent Argaud1, Odile Gateau-Roesch, Lara Chalabreysse

  • 1INSERM E0226, Laboratoire de Physiologie Lyon-Nord, Université Claude Bernard Lyon I, 8, Avenue Rockefeller, 69373 Lyon, France. laurent.argaud@chu-lyon.fr

Cardiovascular Research
|January 21, 2004
PubMed
Summary

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Climate-induced shifts in cod spawning phenology across the North Atlantic.

Scientific reports·2026
Same author

Individual variability in activity patterns in Atlantic halibut (Hippoglossus hippoglossus) revealed using pop-up satellite tags.

Journal of fish biology·2026
Same author

Moving Beyond Morphology: Toward a Morpho-Molecular Classification of Pleural Mesothelioma.

Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer·2026
Same author

Comprehensive pathogen diagnostics in wild fish populations using blood-based molecular strategies: an Atlantic herring case study.

Scientific reports·2025
Same author

Microplastic contamination in fish from the St. Lawrence River and Estuary: Roles of semisynthetic polymers, passive uptake, and wastewater inputs.

Environmental research·2025
Same author

Recurrence of Solitary Fibrous Tumour of the Pleura: A 20-Years Bi-centric Study with Risk Score Comparison.

European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery·2025

Ischemic preconditioning (PC) delays mitochondrial permeability transition (MPT) pore opening, reducing infarct size and cardiomyocyte apoptosis. This suggests MPT pore opening plays a key role in the protective effects of PC.

Area of Science:

  • Cardiovascular Research
  • Mitochondrial Biology
  • Ischemic Physiology

Background:

  • Ischemic preconditioning (PC) is a phenomenon where brief exposure to ischemia protects against subsequent longer ischemic insults.
  • Mitochondrial permeability transition (MPT) pore opening is implicated in cell death during ischemia-reperfusion injury.
  • The precise mechanisms by which PC confers protection are not fully elucidated.

Purpose of the Study:

  • To investigate the role of mitochondrial permeability transition (MPT) pore opening in ischemic preconditioning (PC).
  • To determine if PC modifies the threshold for MPT pore opening.
  • To assess the impact of MPT pore inhibitors on infarct size and apoptosis in the context of PC.

Main Methods:

  • New Zealand White rabbits were subjected to protocols involving ischemia-reperfusion with or without PC.

Related Experiment Videos

  • Mitochondria were isolated to assess Ca(2+)-induced MPT pore opening.
  • Animals were pretreated with saline, cyclosporin A (CsA), or Cs29 (MPT pore inhibitor).
  • Infarct size and cardiomyocyte apoptosis were evaluated after prolonged ischemia-reperfusion.

    • Main Results:

    • PC significantly increased the Ca(2+) overload required for MPT pore opening compared to controls.
    • MPT pore inhibitors (CsA and Cs29) also increased the Ca(2+) threshold for MPT.
    • PC and MPT pore inhibitors reduced infarct size and cardiomyocyte apoptosis.
    • PC hearts showed reduced infarct size (15%) compared to controls (55%), while CsA/Cs29 treatment resulted in 25% infarct size.

    Conclusions:

    • Delayed opening of the MPT pore appears to be a critical mechanism underlying the cardioprotective effects of ischemic preconditioning.
    • Inhibiting MPT pore opening mimics and enhances the protective effects of PC.
    • Targeting the MPT pore represents a potential therapeutic strategy for mitigating ischemia-reperfusion injury.