The Role of Thrombin in Brain Injury After Hemorrhagic and Ischemic Stroke.
Cerebral hemorrhage
Cerebral ischemia
Intraventricular hemorrhage
Neuroinflammation
Subarachnoid hemorrhage
Thrombin
Thrombin receptors
Journal
Translational stroke research
ISSN: 1868-601X
Titre abrégé: Transl Stroke Res
Pays: United States
ID NLM: 101517297
Informations de publication
Date de publication:
06 2021
06 2021
Historique:
received:
24
07
2020
accepted:
23
09
2020
revised:
22
09
2020
pubmed:
30
9
2020
medline:
14
1
2022
entrez:
29
9
2020
Statut:
ppublish
Résumé
Thrombin is increased in the brain after hemorrhagic and ischemic stroke primarily due to the prothrombin entry from blood either with a hemorrhage or following blood-brain barrier disruption. Increasing evidence indicates that thrombin and its receptors (protease-activated receptors (PARs)) play a major role in brain pathology following ischemic and hemorrhagic stroke (including intracerebral, intraventricular, and subarachnoid hemorrhage). Thrombin and PARs affect brain injury via multiple mechanisms that can be detrimental or protective. The cleavage of prothrombin into thrombin is the key step of hemostasis and thrombosis which takes place in every stroke and subsequent brain injury. The extravascular effects and direct cellular interactions of thrombin are mediated by PARs (PAR-1, PAR-3, and PAR-4) and their downstream signaling in multiple brain cell types. Such effects include inducing blood-brain-barrier disruption, brain edema, neuroinflammation, and neuronal death, although low thrombin concentrations can promote cell survival. Also, thrombin directly links the coagulation system to the immune system by activating interleukin-1α. Such effects of thrombin can result in both short-term brain injury and long-term functional deficits, making extravascular thrombin an understudied therapeutic target for stroke. This review examines the role of thrombin and PARs in brain injury following hemorrhagic and ischemic stroke and the potential treatment strategies which are complicated by their role in both hemostasis and brain.
Identifiants
pubmed: 32989665
doi: 10.1007/s12975-020-00855-4
pii: 10.1007/s12975-020-00855-4
pmc: PMC8005504
mid: NIHMS1633256
doi:
Substances chimiques
Thrombin
EC 3.4.21.5
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
496-511Subventions
Organisme : NINDS NIH HHS
ID : R01 NS096917
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS106746
Pays : United States
Organisme : NINDS NIH HHS
ID : R21 NS112394
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS090925
Pays : United States
Organisme : NINDS NIH HHS
ID : R35 NS116786
Pays : United States
Organisme : NINDS NIH HHS
ID : NS-116786
Pays : United States
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