Related Experiment Video
Updated: Jun 28, 2026

Oxygen-Glucose Deprivation and Reoxygenation as an In Vitro Ischemia-Reperfusion Injury Model for Studying Blood-Brain Barrier Dysfunction
Published on: May 7, 2015
Gap junctions as therapeutic targets in brain injury following hypoxia-ischemia
Macarena Sahores1, Ariadna Mendoza-Naranjo
1Department of Cell and Developmental Biology, University College London, London WC1E 6BT, UK. m.sahores@ucl.ac.uk
Abstract:
Gap junctions (GJs) are highly specialized membrane structures which allow the passage of small molecules and ions between neighboring cells. Intercellular communication via GJs is a crucial mechanism that plays a central role in several pathologies. This review focuses on: i) the role of connexins (Cxs, transmembrane proteins that form GJ channels) in the pathophysiology of neuronal injury after brain hypoxia-ischemia, ii) the opposing theories regarding whether Cxs are protective agents or contribute to the spread of damage, and iii) recent patent applications and registrations showing Cxs as key targets in regulating GJ-mediated intercellular communication.
Related Concept Videos
Gap Junctions
Gap Junctions
Ischemic Stroke ll: Pathophysiology
The Blood-brain Barrier
Overview of Synapses
Overview of Cell-Cell Junctions
Occluding or Tight Junctions
Tight...

