Abstract
Two decades into the two thousands, intracerebral hemorrhagic stroke (ICH) continues to reap lives across the globe. In the US, nearly 12,000 people suffer from ICH every year. Half of them survive, but many are left with permanent physical and cognitive disabilities, the severity of which depends on the location and broadness of the brain region affected by the hemorrhage. The ongoing efforts to identify risk factors for hemorrhagic stroke have been instrumental for the development of new medical practices to prevent, aid the recovery and reduce the risk of recurring ICH. Recent efforts approach the study of ICH from a different angle, providing information on how we can limit brain damage by manipulating astrocyte receptors. These results provide a novel understanding of how astrocytes contribute to brain injury and recovery from small ICH. Here, we discuss current knowledge on the risk factors and molecular pathology of ICH and the functional properties of astrocytes and their role in ICH. Last, we discuss candidate astrocyte receptors that may prove to be valuable therapeutic targets to treat ICH. Together, these findings provide basic and clinical scientists useful information for the future development of strategies to improve the detection of small ICH, limit brain damage, and prevent the onset of more severe episodes of brain hemorrhage.
Highlights
Preserving the function of the brain throughout the course of a lifetime is a challenging task that requires the coordinated efforts of healthy neurons, glial cells, and blood vessels
We summarize the current knowledge on the risk factors for intracerebral hemorrhagic stroke (ICH) and discuss how astrocytes could contribute to limit brain damage caused by ICH
Recent advances in high-throughput genotyping technologies, big data analysis, genome-wide association studies, and the creation of large international consortia [25] have led to the identification of genetic risk factors that vary depending on the brain region affected by ICH [26, 27]
Summary
Preserving the function of the brain throughout the course of a lifetime is a challenging task that requires the coordinated efforts of healthy neurons, glial cells, and blood vessels. Glial reactivity has been well documented in pathological studies of ICH, the structural and functional changes associated with it were initially interpreted as representing a downstream effect or a “reactive” response to neuronal damage [1]. Recent evidence challenges this interpretation suggesting that glial cells are “active” contributors to brain damage, meaning that glial pathology is part of the disease progression. Through the activity of K+ channels (e.g., Kir4.1), astrocytes maintain the extracellular K+ concentration at levels that are compatible with life [4, 5] Through their aquaporin-rich endfeet at the cerebral capillaries, astrocytes control the bidirectional movement of water across the cell membrane [5].
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