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Related Concept Videos

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...

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CaMKIIα as a Promising Drug Target for Ischemic Grey Matter.

Nane Griem-Krey1, Andrew N Clarkson2, Petrine Wellendorph1

  • 1Department of Drug Design and Pharmacology, University of Copenhagen, 2100 Copenhagen, Denmark.

Brain Sciences
|December 23, 2022
PubMed
Summary

Targeting Ca2+/calmodulin-dependent protein kinase II (CaMKII) after ischemic stroke offers neuroprotection. New strategies aim to specifically inhibit pathological CaMKII activity, avoiding interference with essential physiological functions.

Keywords:
CaMKIIGHB analoguesHOCPCAexcitotoxicityglutamateischemianeuroprotectionstroke

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Ca2+/calmodulin-dependent protein kinase II (CaMKII) is crucial for Ca2+-dependent signaling, particularly CaMKIIα in neurons.
  • CaMKIIα integrates glutamate signals and is implicated in ischemic stroke-related cell death.
  • Broad CaMKII inhibition is problematic due to its role in vital physiological processes like synaptic plasticity.

Purpose of the Study:

  • To review recent advances in understanding CaMKII's role in ischemia.
  • To explore strategies for pathospecific pharmacological targeting of CaMKII signaling after ischemic stroke.

Main Methods:

  • Review of existing literature on CaMKII function and dysfunction in ischemic conditions.
  • Discussion of direct and indirect pharmacological targeting strategies for CaMKII.

Main Results:

  • Ischemia affects CaMKII activity, contributing to cell death.
  • Direct targeting involves inhibiting CaMKII kinase activity.
  • Indirect targeting focuses on modulating the CaMKIIα association (hub) domain.

Conclusions:

  • Pathospecific targeting of CaMKII is necessary to balance neuroprotection with preservation of physiological functions.
  • Peptide inhibitors offer direct kinase activity modulation.
  • γ-hydroxybutyrate (GHB) analogues show potential for indirect targeting via the hub domain.