Sphingosine-1-phosphate Signalling in Aneurysmal Subarachnoid Haemorrhage: Basic Science to Clinical Translation.

Autor: Gaastra B; Faculty of Medicine, University of Southampton, Southampton, SO17 1BJ, UK. b.gaastra@soton.ac.uk.; Department of Neurosurgery, Wessex Neurological Centre, University Hospital Southampton, Southampton, SO16 6YD, UK. b.gaastra@soton.ac.uk., Zhang J; Center of Neuroscience Research, Loma Linda University, Loma Linda, CA, 92350, USA., Tapper W; Faculty of Medicine, University of Southampton, Southampton, SO17 1BJ, UK., Bulters D; Department of Neurosurgery, Wessex Neurological Centre, University Hospital Southampton, Southampton, SO16 6YD, UK., Galea I; Faculty of Medicine, University of Southampton, Southampton, SO17 1BJ, UK.
Jazyk: angličtina
Zdroj: Translational stroke research [Transl Stroke Res] 2024 Apr; Vol. 15 (2), pp. 352-363. Date of Electronic Publication: 2023 Feb 07.
DOI: 10.1007/s12975-023-01133-9
Abstrakt: Sphingosine-1-phosphate (S1P) is generated intracellularly and, when transported to the extracellular compartment, predominantly signals through S1P receptors. The S1P signalling pathway has been implicated in the pathophysiology of neurological injury following aneurysmal subarachnoid haemorrhage (aSAH). In this review, we bring together all the available data regarding the role of S1P in neurological injury following aSAH. There is agreement in the literature that S1P increases in the cerebrospinal fluid following aSAH and leads to cerebral artery vasospasm. On the other hand, the role of S1P in the parenchyma is less clear cut, with different studies arguing for beneficial and deleterious effects. A parsimonious interpretation of this apparently conflicting data is presented. We discuss the potential of S1P receptor modulators, in clinical use for multiple sclerosis, to be repurposed for aSAH. Finally, we highlight the gaps in our knowledge of S1P signalling in humans, the clinical challenges of targeting the S1P pathway after aSAH and other research priorities.
(© 2023. The Author(s).)
Databáze: MEDLINE
Externí odkaz: