Abstract
Cerebral edema often manifests after the development of cerebrovascular disease, particularly in the case of stroke, both ischemic and hemorrhagic. Without clinical intervention, the influx of water into brain tissues leads to increased intracranial pressure, cerebral herniation, and ultimately death. Strategies to manage the development of edema constitute a major unmet therapeutic need. However, despite its major clinical significance, the mechanisms underlying cerebral water transport and edema formation remain elusive. Aquaporins (AQPs) are a class of water channel proteins which have been implicated in the regulation of water homeostasis and cerebral edema formation, and thus represent a promising target for alleviating stroke-induced cerebral edema. This review examines the significance of relevant AQPs in stroke injury and subsequently explores neuroprotective strategies aimed at modulating AQP expression, with a particular focus on AQP4, the most abundant AQP in the central nervous system.
Highlights
Stroke constitutes a major global health problem, being the second leading cause of death worldwide, and the foremost cause of neurological disability in the United States
A population of AQP1-expressing astrocytes was recently discovered in the white matter and glia limitans in the brains of non-human primates. This astrocyte population is absent in the rodent brain, indicating that AQP1 expression differs among species [3,6,7] Under pathological conditions, these astrocytic AQP1 channels are thought to have a complementary role to AQP4 in regulating brain water homeostasis
Unlike AQP4, which is localized to astrocytic endfeet, AQP9 is found dispersed throughout astrocytic cell bodies and processes
Summary
Stroke constitutes a major global health problem, being the second leading cause of death worldwide, and the foremost cause of neurological disability in the United States. Ischemic stroke accounts for 80% of stroke cases, and occurs as a result of cerebral vessel occlusion due to a thrombus or embolus. Hemorrhagic stroke involves the rupturing of a vessel, causing the leakage of blood into the parenchyma. Cerebral edema development often accompanies both ischemic infarct and intracerebral hemorrhage (ICH), but the mechanism underlying edema formation differs between the two types of stroke. Brain edema results in increased intracranial pressure, decreased blood flow, and ischemia, and is correlated with poor patient outcomes and a greater incidence of mortality. The only approved therapies for treating cerebral edema include decompressive craniectomy and osmotherapy, which both aim to alleviate downstream effects, rather than addressing the molecular mechanisms underlying edema development [2]
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