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Neurovascular Events After Subarachnoid Hemorrhage: Focusing on Subcellular Organelles

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Neurovascular Events After Subarachnoid Hemorrhage

Part of the book series: Acta Neurochirurgica Supplement ((NEUROCHIRURGICA,volume 120))

Abstract

Subarachnoid hemorrhage (SAH) is a devastating condition with high morbidity and mortality rates due to the lack of effective therapy. Early brain injury (EBI) and cerebral vasospasm (CVS) are the two most important pathophysiological mechanisms for brain injury and poor outcomes for patients with SAH. CVS has traditionally been considered the sole cause of delayed ischemic neurological deficits after SAH. However, the failure of antivasospastic therapy in patients with SAH supported changing the research target from CVS to other mechanisms. Currently, more attention has been focused on global brain injury within 3 days after ictus, designated as EBI. The dysfunction of subcellular organelles, such as endoplasmic reticulum stress, mitochondrial failure, and autophagy–lysosomal system activation, has developed during EBI and delayed brain injury after SAH. To our knowledge, there is a lack of review articles addressing the direction of organelle dysfunction after SAH. In this review, we discuss the roles of organelle dysfunction in the pathogenesis of SAH and present the opportunity to develop novel therapeutic strategies of SAH via modulating the functions of organelles.

The authors Sheng Chen and Haijian Wu contributed equally to this work.

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Acknowledgement

This study was supported by a National Institutes of Health grant (NS053407) to JH Zhang and by a National Natural Science Foundation of China grant (No.81171096) to JM Zhang.

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We declare that we have no conflict of interest.

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Chen, S., Wu, H., Tang, J., Zhang, J., Zhang, J.H. (2015). Neurovascular Events After Subarachnoid Hemorrhage: Focusing on Subcellular Organelles. In: Fandino, J., Marbacher, S., Fathi, AR., Muroi, C., Keller, E. (eds) Neurovascular Events After Subarachnoid Hemorrhage. Acta Neurochirurgica Supplement, vol 120. Springer, Cham. https://doi.org/10.1007/978-3-319-04981-6_7

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