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Open AccessJournal ArticleDOI

Cerebral edema after ischemic stroke: Pathophysiology and underlying mechanisms

TLDR
This review discusses the classification and pathological characteristics of cerebral edema, the possible relationship of the development of cerebral Edema after ischemic stroke with aquaporin 4, the SUR1-TRPM4 channel, matrix metalloproteinase 9, microRNA, cerebral venous reflux, inflammatory reactions, and cerebral ischemia/reperfusion injury.
Abstract
Ischemic stroke is associated with increasing morbidity and has become the main cause of death and disability worldwide. Cerebral edema is a serious complication arising from ischemic stroke. It causes an increase in intracranial pressure, rapid deterioration of neurological symptoms, and formation of cerebral hernia, and is an important risk factor for adverse outcomes after stroke. To date, the detailed mechanism of cerebral edema after stroke remains unclear. This limits advances in prevention and treatment strategies as well as drug development. This review discusses the classification and pathological characteristics of cerebral edema, the possible relationship of the development of cerebral edema after ischemic stroke with aquaporin 4, the SUR1-TRPM4 channel, matrix metalloproteinase 9, microRNA, cerebral venous reflux, inflammatory reactions, and cerebral ischemia/reperfusion injury. It also summarizes research on new therapeutic drugs for post-stroke cerebral edema. Thus, this review provides a reference for further studies and for clinical treatment of cerebral edema after ischemic stroke.

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Nitric Oxide/Nitric Oxide Synthase System in the Pathogenesis of Neurodegenerative Disorders—An Overview

TL;DR: In this article , the authors present the main causes of increased pathological production, as well as the most important pathophysiological mechanisms triggered by nitric oxide, mechanisms that could help explain a part of the complex picture of neurodegenerative diseases and help develop targeted therapies.
Journal ArticleDOI

Bilobalide Protects Pheochromocytoma Cell from Oxygen-Glucose Deprivation/Reperfusion Induced Injury via Activating Wnt1/Beta Catenin Pathway

TL;DR: Yu et al. as mentioned in this paper explored the protective effect of bilobalide on the pheochromocytoma cell injury induced by oxygen-glucose deprivation/reperfusion in vitro.
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Low Temperature Delays the Effects of Ischemia in Bergmann Glia and in Cerebellar Tissue Swelling

TL;DR: In this article, the neuroprotective role of lowering the temperature in ischemia mimicked by an episode of oxygen and glucose deprivation (OGD) in mouse cerebellar slices was investigated.
Journal ArticleDOI

Pharmacodynamic evaluation of Cordyceps sinensis (Berk.) Sacc. for ischemic stroke in rats and potential mechanism through network pharmacology and molecular docking

TL;DR: In this paper , the authors explored the therapeutic potential of Cordyceps sinensis (Berk.) Sacc. (C. sinensis, Dong Chong Xia Cao) in an ischemic stroke (IS) model and predict its possible mechanism through network pharmacology.
Book ChapterDOI

Hypoxia Responsive Nanomaterials for Cerebral Ischemia Diagnosis

TL;DR: In this paper , a comprehensive pathology of cerebral ischemia and its related maladies, a brief emphasis towards available diagnosis methods, an introduction of the concept of nanotechnology as a novel diagnostic tool towards early identification of cerebral waschemia, and finally available treatment strategies are discussed.
References
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Journal ArticleDOI

The role of microRNA-1 and microRNA-133 in skeletal muscle proliferation and differentiation

TL;DR: The results show that two mature miRNAs, derived from the same miRNA polycistron and transcribed together, can carry out distinct biological functions and suggest a molecular mechanism in which miRN as participate in transcriptional circuits that control skeletal muscle gene expression and embryonic development.
Journal ArticleDOI

Ischemia and reperfusion—from mechanism to translation

TL;DR: Ischemia and reperfusion-elicited tissue injury contributes to morbidity and mortality in a wide range of pathologies, including myocardial infarction, ischemic stroke, acute kidney injury, trauma, circulatory arrest, sickle cell disease and sleep apnea as discussed by the authors.
Journal ArticleDOI

On the Absorption of Fluids from the Connective Tissue Spaces

TL;DR: It is inquired whether the blood vessels do absorb such isotonic fluids, and the manner in which this absorption takes place.
Journal ArticleDOI

VEGF enhances angiogenesis and promotes blood-brain barrier leakage in the ischemic brain

TL;DR: VEGF can markedly enhance angiogenesis in the ischemic brain and reduce neurological deficits during stroke recovery and that inhibition of VEGF at the acute stage of stroke may reduce the BBB permeability and the risk of hemorrhagic transformation after focal cerebral ischemia.
Trending Questions (1)
How does brain edema after stroke occur?

The paper discusses that the detailed mechanism of cerebral edema after stroke remains unclear, limiting advances in prevention and treatment strategies.