Related Experiment Video

Updated: May 9, 2026

A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion
13:42

A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion

Published on: July 17, 2012

[Protein kinases role in adaptive phenomenon of heart ischemic postconditioning development]

L N Maslov, A G Mrochek, I A Shchepetkin

    Rossiiskii Fiziologicheskii Zhurnal Imeni I.M. Sechenova
    |July 19, 2013
    PubMed

    Insights

    Protein kinases play a role in heart protection after ischemia. Further research is needed to clarify the exact contributions of specific kinases like mTOR and GSK3b in limiting infarct size.

    Area of Science:

    • Cardiovascular Research
    • Molecular Biology
    • Biochemistry

    Context:

    • Ischemic heart disease remains a leading cause of mortality worldwide.
    • Postconditioning is a protective strategy against ischemia-reperfusion injury.
    • Protein kinases are crucial signaling molecules in cellular processes.

    Purpose:

    • To review and analyze the involvement of protein kinases in the signaling pathways of cardiac ischemic postconditioning.
    • To identify established and potential kinase targets within postconditioning mechanisms.
    • To highlight areas requiring further investigation in kinase signaling for cardioprotection.

    Summary:

    • Literature analysis confirms involvement of protein kinases (PKC, PI3K, Akt, MEK1/2, ERK1/2, mTOR, p70s6K, GSK3b, PKG) and associated molecules (eNOS, NO, GC, mitoKATP, ROS, MPT pore) in postconditioning.
    • The precise roles of mTOR, p70s6K, AMPK, and GSK3b in infarct size limitation remain unclear.
    • Further studies are necessary to elucidate signaling events following JAK2 and p38 kinase activation, and the hypothetical roles of Ras and Raf-1.

    Impact:

    • Clarifies the complex signaling network underlying cardiac postconditioning.
    • Identifies specific protein kinases as potential therapeutic targets for mitigating myocardial infarction.
    • Guides future research directions to enhance understanding and application of postconditioning strategies.

    More Related Videos

    Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury07:23

    Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury

    Published on: March 7, 2022

    Remote Limb Ischemic Preconditioning: A Neuroprotective Technique in Rodents07:52

    Remote Limb Ischemic Preconditioning: A Neuroprotective Technique in Rodents

    Published on: June 2, 2015

    Related Concept Videos

    Heart Failure II: Pathophysiology01:29

    Heart Failure II: Pathophysiology

    Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
    Pathophysiology of Heart Failure01:17

    Pathophysiology of Heart Failure

    Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
    Cellular Adaptation II: Hypertrophy01:26

    Cellular Adaptation II: Hypertrophy

    Hypertrophy is the increase in the size of individual cells, resulting in the enlargement of a tissue or organ. Unlike hyperplasia, which involves an increase in cell number, hypertrophy is characterized by an increase in cell volume. This process often occurs in response to higher functional demand or hormonal stimulation, leading to the production of more structural proteins and organelles, thereby enhancing the cells' work capacity.There are two primary types of hypertrophy: physiological...
    Protein Kinases and Phosphatases02:54

    Protein Kinases and Phosphatases

    Proteins undergo chemical modifications that trigger changes in the charge, structure, and conformation of the proteins. Phosphorylation, acetylation, glycosylation, nitrosylation, ubiquitination, lipidation, methylation, and proteolysis are various protein modifications that regulate protein activity. Such modifications are usually enzyme-driven.
    Protein kinases
    Many proteins in the cell are regulated by phosphorylation, the addition of a phosphate group. A family of enzymes called kinases...
    Ischemic Heart Disease: Overview01:17

    Ischemic Heart Disease: Overview

    Ischemic heart disease occurs when the heart's blood supply dwindles, causing an ominous lack of oxygen and nutrients. This deficiency, stemming from reduced or obstructed blood flow, spells danger, leading to heart muscle damage and dysfunction.
    Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and narrowing...
    cAMP-dependent Protein Kinase Pathways01:25

    cAMP-dependent Protein Kinase Pathways

    Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...