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

Prevention of the ischemia-induced decrease in mitochondrial Tom20 content by ischemic preconditioning.

Kerstin Boengler1, Petra Gres, Alberto Cabestrero

  • 1Institut für Pathophysiologie, Universitätsklinikum Essen, Germany.

Journal of Molecular and Cellular Cardiology
|July 11, 2006
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

Extracellular RNA drives TNF-α/TNF-receptor-1 mediated cardiac ischemia/reperfusion injury: Mechanistic insights and therapeutic potential of RNase1.

Pharmacological research·2025
Same author

Optimal opportunistic screening of atrial fibrillation using pulse palpation in cardiology outpatient clinics: Who and how.

PloS one·2022
Same author

Life-threatening arrhythmias in anterior ST-segment elevation myocardial infarction patients treated by percutaneous coronary intervention: adverse impact of morphine.

European heart journal. Acute cardiovascular care·2021
Same author

Correction: PLGA protein nanocarriers with tailor-made fluorescence/MRI/PET imaging modalities.

Nanoscale·2021
Same author

Effect of COMBinAtion therapy with remote ischemic conditioning and exenatide on the Myocardial Infarct size: a two-by-two factorial randomized trial (COMBAT-MI).

Basic research in cardiology·2021
Same author

Predictive value of early cardiac magnetic resonance imaging functional and geometric indexes for adverse left ventricular remodelling in patients with anterior ST-segment elevation myocardial infarction: A report from the CIRCUS study.

Archives of cardiovascular diseases·2020
Same journal

Large extracellular vesicles derived from red blood cells in coronary artery disease patients with anemia promote endothelial dysfunction.

Journal of molecular and cellular cardiology·2026
Same journal

SnRNA-seq identifies FN1-SDC4 axis triggering epicardial activation in right ventricular remodeling in pulmonary hypertension.

Journal of molecular and cellular cardiology·2026
Same journal

Therapeutic impact of normal dietary patterns on diabetic cardiomyopathy: Transcriptomic and proteomic insights.

Journal of molecular and cellular cardiology·2026
Same journal

Structural, biophysical and cellular assessment of filamin C M82K: A test case for VUS interpretation in cardiomyopathy.

Journal of molecular and cellular cardiology·2026
Same journal

Precision modification of heart failure signaling by CRISPR-Cas9 base editing.

Journal of molecular and cellular cardiology·2026
Same journal

Retraction notice to 'Sam68 impedes the recovery of arterial injury by augmenting inflammatory response' [Journal of Molecular and Cellular Cardiology 137 (2019) 82-92].

Journal of molecular and cellular cardiology·2026
See all related articles

Ischemic preconditioning preserves mitochondrial Tom20 protein levels after heart ischemia/reperfusion injury. This preservation may improve mitochondrial function and cell survival, reducing infarct size.

Area of Science:

  • Cardiovascular Biology
  • Mitochondrial Physiology
  • Cellular Stress Response

Background:

  • Mitochondrial function is crucial for cell survival after ischemia/reperfusion (I/R).
  • Mitochondrial protein import via TOM and TIM complexes is essential for function.
  • Ischemic preconditioning (IP) improves mitochondrial resilience to I/R.

Purpose of the Study:

  • To investigate the impact of I/R and IP on mitochondrial protein import machinery.
  • To analyze the expression of Tom20, Tom40, and Tim23 in response to I/R with and without IP.

Main Methods:

  • Utilized a Goettinger minipig model of myocardial I/R.
  • Applied ischemic preconditioning (10 min ischemia/15 min reperfusion) prior to 90 min low-flow ischemia.
  • Isolated mitochondria from control, ischemic, and preconditioned myocardium.

Related Experiment Videos

  • Quantified mitochondrial protein levels (Tom20, Tom40, Tim23, ANT) using Western blot analysis.

    • Main Results:

    • IP significantly reduced infarct size (20.1% vs. 6.5% of area at risk).
    • Mitochondrial Tom20 content was reduced by I/R but preserved by IP (0.72 vs. 1.17 arbitrary units).
    • Mitochondrial Tom40, Tim23, and ANT levels remained unchanged by I/R or IP.

    Conclusions:

    • Mitochondrial Tom20 protein levels are specifically preserved by ischemic preconditioning following I/R injury.
    • This preservation of Tom20 may contribute to improved mitochondrial function and enhanced cell survival.
    • Targeting mitochondrial import components like Tom20 could be a therapeutic strategy for I/R injury.