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

GPCR Desensitization01:12

GPCR Desensitization

G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
The Two-State Receptor Model01:29

The Two-State Receptor Model

The two-state receptor model explains a drug's interaction with receptors, such as G protein-coupled receptors and ligand-gated ion channels, to induce or inhibit a biological response. When no natural ligands are present, a receptor exists in an equilibrium of inactive (Ri) and active (Ra) conformations. The inactive form does not produce a response, while the active form generates a basal effect known as constitutive activity.
The binding affinity of a drug determines its interaction with one...
Desensitization and Tachyphylaxis01:20

Desensitization and Tachyphylaxis

Tachyphylaxis is described as a rapid decrease in response to a drug after repeated or continuous administration of the same drug dose. It is a phenomenon where the body becomes less responsive to a particular substance or intervention over time, requiring higher doses or stronger interventions to achieve the same effect. It results from adaptive changes in the body's receptors, signaling pathways, or physiological processes that occur in response to prolonged exposure to a stimulus.
Several...
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Chemical Synapses01:26

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Chemical Synapses01:26

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...

You might also read

Related Articles

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

Sort by
Same author

Initial Despair and Current Hope of Identifying a Clinically Useful Treatment of Myocardial Reperfusion Injury: Insights Derived from Studies of Platelet P2Y<sub>12</sub> Antagonists and Interference with Inflammation and NLRP3 Assembly.

International journal of molecular sciences·2024
Same author

Automated segmentation of the left-ventricle from MRI with a fully convolutional network to investigate CTRCD in breast cancer patients.

Journal of medical imaging (Bellingham, Wash.)·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

Gamma secretase activating protein promotes end-organ dysfunction after bacterial pneumonia.

American journal of physiology. Lung cellular and molecular physiology·2023
Same author

Lethal Caspase-1/4-Dependent Injury Occurs in the First Minutes of Coronary Reperfusion and Requires Calpain Activity.

International journal of molecular sciences·2023
Same author

Can global longitudinal strain (GLS) with magnetic resonance prognosticate early cancer therapy-related cardiac dysfunction (CTRCD) in breast cancer patients, a prospective study?

Magnetic resonance imaging·2022
Same journal

Inflammation Impairs Poststroke Recovery by Disrupting Iron Homeostasis in Brain.

Antioxidants & redox signaling·2026
Same journal

Histone Lactylation Links Glycolysis to Ferroptosis in Diabetic Cataract.

Antioxidants & redox signaling·2026
Same journal

Insights into the Multifaceted Roles of 3-Mercaptopyruvate Sulfurtransferase in Liver Diseases.

Antioxidants & redox signaling·2026
Same journal

NINJ1 Aggravates Doxorubicin-Induced Cardiotoxicity by Suppressing AMPK-Mediated HIF-1α Deubiquitination.

Antioxidants & redox signaling·2026
Same journal

<i>Corrigendum to:</i> Suppression of Cardiac Autophagy by Hyperinsulinemia in Insulin Receptor-Deficient Hearts Is Mediated by Insulin-Like Growth Factor Receptor Signaling.

Antioxidants & redox signaling·2026
Same journal

Sleeve Gastrectomy Is Associated with Improved Systemic Redox Homeostasis in T2DM Through Ghrelin-GHSR Attenuation, POMC Neuronal Modulation, and CD4<sup>+</sup> T Cell Metabolic Reprogramming.

Antioxidants & redox signaling·2026
See all related articles

Related Experiment Video

Updated: Jun 12, 2026

Remote Limb Ischemic Preconditioning: A Neuroprotective Technique in Rodents
07:52

Remote Limb Ischemic Preconditioning: A Neuroprotective Technique in Rodents

Published on: June 2, 2015

Ischemic postconditioning: from receptor to end-effector.

Michael V Cohen1, James M Downey

  • 1Department of Physiology, College of Medicine, University of South Alabama, Mobile, AL 36688, USA. mcohen@usouthal.edu

Antioxidants & Redox Signaling
|June 4, 2010
PubMed
Summary
This summary is machine-generated.

Ischemic postconditioning protects the heart after reperfusion injury by maintaining acidosis to prevent mitochondrial permeability transition pore formation. This signaling pathway activates protective mechanisms, ultimately salvaging cells from necrosis.

More Related Videos

Bilateral Common Carotid Artery Occlusion as an Adequate Preconditioning Stimulus to Induce Early Ischemic Tolerance to Focal Cerebral Ischemia
07:46

Bilateral Common Carotid Artery Occlusion as an Adequate Preconditioning Stimulus to Induce Early Ischemic Tolerance to Focal Cerebral Ischemia

Published on: May 9, 2013

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
05:26

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction

Published on: May 28, 2019

Related Experiment Videos

Last Updated: Jun 12, 2026

Remote Limb Ischemic Preconditioning: A Neuroprotective Technique in Rodents
07:52

Remote Limb Ischemic Preconditioning: A Neuroprotective Technique in Rodents

Published on: June 2, 2015

Bilateral Common Carotid Artery Occlusion as an Adequate Preconditioning Stimulus to Induce Early Ischemic Tolerance to Focal Cerebral Ischemia
07:46

Bilateral Common Carotid Artery Occlusion as an Adequate Preconditioning Stimulus to Induce Early Ischemic Tolerance to Focal Cerebral Ischemia

Published on: May 9, 2013

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
05:26

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction

Published on: May 28, 2019

Area of Science:

  • Cardiovascular Physiology
  • Cellular Signaling
  • Mitochondrial Biology

Background:

  • Ischemic preconditioning is effective but requires preemptive application.
  • Ischemic postconditioning offers cardioprotection during reperfusion, relevant to procedures like angioplasty.
  • Understanding postconditioning's signaling pathways is key to developing pharmacological interventions.

Purpose of the Study:

  • To investigate the signaling mechanisms of ischemic postconditioning.
  • To identify potential pharmacological triggers for cardioprotection without angioplasty.
  • To elucidate the role of mitochondrial permeability transition pores (MPTPs) in cell death and salvage.

Main Methods:

  • Examining cellular pH changes during reperfusion.
  • Investigating the role of acidosis in MPTP formation.
  • Analyzing the signaling cascade involving reactive oxygen species, protein kinase C, adenosine receptors, phosphatidylinositol 3-kinase, Akt, and nitric oxide synthase.

Main Results:

  • Reperfusion leads to intracellular acidosis, which initially inhibits MPTP formation.
  • Signaling pathways activated during postconditioning generate endogenous MPTP antagonists.
  • Key signaling molecules include protein kinase C, adenosine A(2b) receptors, phosphatidylinositol 3-kinase/Akt, and nitric oxide synthase, culminating in MPTP inhibition.

Conclusions:

  • Ischemic postconditioning utilizes a complex signaling network to protect cells from reperfusion injury.
  • Maintaining acidosis is crucial for initiating protective signaling and preventing MPTP-mediated necrosis.
  • Targeting this pathway could lead to novel pharmacological cardioprotective therapies.