Neural Regeneration Research ›› 2022, Vol. 17 ›› Issue (4): 783-784.doi: 10.4103/1673-5374.322456

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Involvement of glucose transporter overexpression in the protection or damage after ischemic stroke

Iván Alquisiras-Burgos, Penélope Aguilera*   

  1. Laboratorio de Patología Vascular Cerebral, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Insurgentes Sur #3877, Col. La Fama, Tlalpan, Ciudad de México, México
  • Online:2022-04-15 Published:2021-10-16
  • Contact: Penélope Aguilera, PhD, penelope.aguilera@innn.edu.mx.
  • Supported by:
    The present work was supported by the CONACYT (CB-2012-01-182266 to PA). Iván Alquisiras Burgos is a doctoral student from Programa de Doctorado en Ciencias Biomédicas, Universidad Nacional Autónoma de México (UNAM) and beneficiary of scholarship No. 275610 from CONACYT. 

Abstract: Cerebral ischemia and resultant energy collapse: The ischemic stroke is a complex neurological condition that can be devastating for patients and their families. This disease is the second leading cause of death worldwide and is characterized by a sudden decrease in cerebral blood flow due to major blood vessel blockage. Ischemic stroke generates two damaged zones with distinctive metabolic characteristics. The first is the ischemic core, the region directly irrigated by the occluded artery. A reduction to less than 20% of the baseline blood flow levels defines the area; therefore, depletion of glucose and adenosine triphosphate (ATP) cause an irreversible failure in the energy metabolism that leads to loss of ionic homeostasis, acidosis, and necrosis. The second is the region surrounding the ischemic core, called the penumbra, characterized by significantly depressed tissue perfusion that is barely sufficient to support basal oxygen, glucose, and ATP levels. The penumbra represents a region at risk that is functionally impaired but potentially recoverable and suitable for neuroregeneration. Therefore, physiological conditions must be reestablished rapidly after ischemia to avoid a permanent metabolic failure in the penumbra.