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Special Issue "Molecular Mechanisms and Pathophysiology of Cerebral Ischemia"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 31 October 2021.

Special Issue Editor

Prof. Moo-Ho Won
E-Mail Website
Guest Editor
Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, Gangwon 24341, Korea
Interests: neurodegeneration; neurogenesis, cerebral ischemia, aging in CNS
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues,

Cerebral ischemia is the leading cause of death worldwide. Despite great efforts to develop potential treatments, the molecular and cellular mechanisms of cerebral ischemia are not fully understood.

Many researchers have been using various animal models of cerebral ischemia with different species of animals, different methods of occlusion of blood vessels, and different periods of occlusion time. The models of cerebral ischemia can be divided into focal and global models. Focal ischemia is characterized by a reduction of cerebral blood flow in a distinct region of the brain, whereas in global ischemia, the reduction of blood flow affects the entire brain or forebrain. Neuronal or tissue damage are different according to the type of ischemic insult. In animal models of global transient cerebral or forebrain ischemia, neuronal damage/death (loss) occurs in vulnerable regions of the brain (i.e., the hippocampus), whereas in animal models of transient focal brain ischemia, neuronal loss occurs when the ischemic duration (damage) is short (mild), or infarction (necrosis) occurs when the ischemic damage (duration) is severe (long). In this regard, the mechanisms of neuronal loss or infarction are apparently different according to the type of ischemic insult.

Diverse mechanisms of pathophysiological events in ischemic damage have been suggested, including the activation of glutamate receptors, a sustained increase in intracellular calcium, oxidative stress caused by free radicals, and the activation of resident microglia related to neuroinflammatory reactions. In addition, the dysfunction of cells related to the blood–brain barrier (BBB), including endothelial cells, astrocytes and pericytes, as well as microglia, is also suggested as a possible mechanism of ischemic injuries.

This Special Issue aims to study the control or modulation of diverse pathways during or after ischemic injuries at the molecular and cellular levels to prevent, attenuate or heal ischemia damage following various brain ischemic insults.

Prof. Moo-Ho Won
Guest Editor

Manuscript Submission Information

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Keywords

  • transient or permanent ischemia
  • neuronal death
  • necrosis
  • inflammation
  • oxidative stress
  • cytotoxicity
  • blood-brain barrier
  • neuroprotection
  • therapeutic strategy

Published Papers (1 paper)

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Research

Open AccessArticle
Ischemia-Reperfusion under Hyperthermia Increases Heme Oxygenase-1 in Pyramidal Neurons and Astrocytes with Accelerating Neuronal Loss in Gerbil Hippocampus
Int. J. Mol. Sci. 2021, 22(8), 3963; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22083963 - 12 Apr 2021
Viewed by 334
Abstract
It has been studied that the damage or death of neurons in the hippocampus is different according to hippocampal subregions, cornu ammonis 1–3 (CA1–3), after transient ischemia in the forebrain, showing that pyramidal neurons located in the subfield CA1 (CA1) are most vulnerable [...] Read more.
It has been studied that the damage or death of neurons in the hippocampus is different according to hippocampal subregions, cornu ammonis 1–3 (CA1–3), after transient ischemia in the forebrain, showing that pyramidal neurons located in the subfield CA1 (CA1) are most vulnerable to this ischemia. Hyperthermia is a proven risk factor for brain ischemia and can develop more severe and extensive brain damage related with mortality rate. It is well known that heme oxygenase-1 (HO-1) activity and expression is increased by various stimuli in the brain, including hyperthermia. HO-1 can be either protective or deleterious in the central nervous system, and its roles depend on the expression levels of enzymes. In this study, we investigated the effects of hyperthermia during ischemia on HO-1 expression and neuronal damage/death in the hippocampus to examine the relationship between HO-1 and neuronal damage/death following 5-min transient ischemia in the forebrain using gerbils. Gerbils were assigned to four groups: (1) sham-operated gerbils with normothermia (Normo + sham group); (2) ischemia-operated gerbils with normothermia (Normo + ischemia group); (3) sham-operated gerbils with hyperthermia (39.5 ± 0.2 °C) during ischemia (Hyper + sham group); and (4) ischemia-operated gerbils with hyperthermia during ischemia (Hyper + ischemia group). HO-1 expression levels in CA1–3 of the Hyper + ischemia group were significantly higher than those in the Normo + ischemia group. HO-1 immunoreactivity in the Hyper + ischemia group was significantly increased in pyramidal neurons and astrocytes with time after ischemia, and the immunoreactivity was significantly higher than that in the Normo + ischemia group. In the Normo + Ischemia group, neuronal death was shown in pyramidal neurons located only in CA1 at 5 days after ischemia. However, in the Hyper + ischemia group, pyramidal neuronal death occurred in CA1–3 at 2 days after ischemia. Taken together, our findings showed that brain ischemic insult during hyperthermic condition brings up earlier and severer neuronal damage/death in the hippocampus, showing that HO-1 expression in neurons and astrocytes is different according to brain subregions and temperature condition. Based on these findings, we suggest that hyperthermia in patients with ischemic stroke must be taken into the consideration in the therapy. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathophysiology of Cerebral Ischemia)
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