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

Ischaemic preconditioning: present position and future directions

D M Yellon1, G F Baxter, D Garcia-Dorado

  • 1Hatter Institute for Cardiovascular Studies, University College London Hospitals, London, UK. s.bush-cavell@ucl.ac.uk

Cardiovascular Research
|April 16, 1998
PubMed
Summary
This summary is machine-generated.

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

Inter-organ communication: pathways and targets to cardioprotection and neuro-protection. A report from the 12th Hatter Cardiovascular Institute workshop.

Basic research in cardiology·2024
Same author

The Infarct-Limiting Effect of Remote Ischemic Conditioning in Rats Is Not Affected by Aspirin.

Cardiovascular drugs and therapy·2023
Same author

Remote ischaemic conditioning: defining critical criteria for success-report from the 11th Hatter Cardiovascular Workshop.

Basic research in cardiology·2022
Same author

Correction: Hearts deficient in both Mfn1 and Mfn2 are protected against acute myocardial infarction.

Cell death & disease·2021
Same author

Targeting myocardial ischaemic injury in the absence of reperfusion.

Basic research in cardiology·2020
Same author

Clinical effects of cyclosporine in acute anterior myocardial infarction complicated by heart failure: A subgroup analysis of the CIRCUS Trial.

American heart journal·2019
Same journal

YAP plays a critical role in myocardial recovery from myocarditis by suppressing IFN-γ signaling pathway.

Cardiovascular research·2026
Same journal

Metabolic crisis and TRPM4 activation cause QT prolongation in TANGO2 deficiency disorder.

Cardiovascular research·2026
Same journal

Personalizing Atrial Fibrillation Therapy: Moving from Genetic Association to Mechanistic Translation.

Cardiovascular research·2026
Same journal

Placental Growth Factor Promotes Endothelial Activation and Inflammatory Remodelling in Pulmonary Hypertension.

Cardiovascular research·2026
Same journal

Endothelial-to-mesenchymal transition (EndMT) in atherosclerosis: mechanisms, models and therapies.

Cardiovascular research·2026
Same journal

The gut-heart axis in cardio-oncology.

Cardiovascular research·2026
See all related articles

Short periods of low blood flow (ischaemia) protect heart muscle cells (myocytes) from damage during a major ischaemic event. This protective adaptation, also seen in other cells, has significant clinical potential.

Area of Science:

  • Cardiology
  • Cellular Physiology
  • Pathophysiology

Background:

  • Myocardial preconditioning involves brief ischaemic episodes that confer protection against subsequent lethal ischaemia.
  • This phenomenon, known as the 'ischaemic tolerance response', is observed in myocytes and other cell types.
  • Understanding this adaptive mechanism is crucial for managing ischaemia-reperfusion injury.

Purpose of the Study:

  • To critically appraise the current knowledge on myocardial preconditioning.
  • To review the pathophysiology of ischaemia-reperfusion injury and cellular metabolic regulation.
  • To identify future research directions in this field.

Main Methods:

  • Literature review and critical analysis of existing research on myocardial preconditioning.

Related Experiment Videos

  • Examination of cellular and molecular mechanisms underlying ischaemic tolerance.
  • Assessment of clinical implications and potential therapeutic applications.

    • Main Results:

    • Myocardial preconditioning significantly delays necrosis following lethal ischaemic insults.
    • The protective adaptation extends beyond cardiac myocytes to various other cell types.
    • Research has expanded our understanding of the pathophysiology of ischaemia-reperfusion injury.

    Conclusions:

    • Myocardial preconditioning is a potent endogenous protective mechanism.
    • Further research is warranted to translate these findings into clinical practice for diverse pathological conditions.
    • A comprehensive appraisal is timely to guide future investigations into cellular metabolism and ischaemia-reperfusion injury.