Acute Ischaemic Stroke: Therapeutic Targets and Key Modulators of the Fibrinolytic System and Clot Formation.
4 affiliations
- 1Department of Neurology, Alfred Hospital, Melbourne, 3004, Australia.
- 2Department of Clinical Neurosciences, School of Translational Medicine, Monash University, Melbourne, Victoria, Australia.
- 3Department of Neurology, Melbourne Brain Centre at the Royal Melbourne Hospital, University of Melbourne, Parkville, Australia.
- 4Australian Centre for Blood Diseases, School of Translational Medicine, Monash University, Melbourne, Victoria, Australia. [email protected].
Abstract
The processes of clot formation and clot dissolution with fibrinolysis underpin the pathophysiological mechanisms of acute ischaemic stroke (AIS) and its treatment. Detailed understanding of the modulation of this system is required to develop effective and safe stroke therapeutics. Clot formation occurs with the interaction of the coagulation cascade, along with platelets and fibrin meshwork. Conversely, fibrinolysis involves the serine protease plasmin, its zymogen, plasminogen and its enzymatic conversion by tissue plasminogen activator. The regulators and inhibitors that modulate the interactions in clot formation and fibrinolysis can be potential targets for new and emerging stroke therapies. The aim of this narrative review is to help inform stroke clinicians and researchers about the role of the fibrinolytic system and its inhibitors in AIS and the potential for new therapeutic targets. We outline the processes involved in clot formation and dissolution, the role of endogenous inhibitors of the fibrinolytic system, followed by potential therapeutic targets including tissue plasminogen activators as well as novel therapies and adjuncts. Better understanding of these processes will provide insight into the variable response to current stroke fibrinolytics amongst AIS patients and help to develop new and improved AIS therapeutics in future.
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BibTeX
@article{swarup2026acute,
title = {{Acute Ischaemic Stroke: Therapeutic Targets and Key Modulators of the Fibrinolytic System and Clot Formation.}},
author = {Oshi Swarup and Anna H Balabanski and Geoffrey C Cloud and Robert L Medcalf},
journal = {Translational stroke research},
year = {2026},
month = oct,
doi = {10.1007/s12975-026-01502-0},
url = {https://europepmc.org/article/MED/42864557},
note = {CC BY},
}
RIS
TY - JOUR
TI - Acute Ischaemic Stroke: Therapeutic Targets and Key Modulators of the Fibrinolytic System and Clot Formation.
AU - Oshi Swarup
AU - Anna H Balabanski
AU - Geoffrey C Cloud
AU - Robert L Medcalf
PY - 2026
DA - 2026/10/13
JO - Translational stroke research
DO - 10.1007/s12975-026-01502-0
UR - https://europepmc.org/article/MED/42864557
AB - The processes of clot formation and clot dissolution with fibrinolysis underpin the pathophysiological mechanisms of acute ischaemic stroke (AIS) and its treatment. Detailed understanding of the modulation of this system is required to develop effective and safe stroke therapeutics. Clot formation occurs with the interaction of the coagulation cascade, along with platelets and fibrin meshwork. Conversely, fibrinolysis involves the serine protease plasmin, its zymogen, plasminogen and its enzymatic conversion by tissue plasminogen activator. The regulators and inhibitors that modulate the interactions in clot formation and fibrinolysis can be potential targets for new and emerging stroke therapies. The aim of this narrative review is to help inform stroke clinicians and researchers about the role of the fibrinolytic system and its inhibitors in AIS and the potential for new therapeutic targets. We outline the processes involved in clot formation and dissolution, the role of endogenous inhibitors of the fibrinolytic system, followed by potential therapeutic targets including tissue plasminogen activators as well as novel therapies and adjuncts. Better understanding of these processes will provide insight into the variable response to current stroke fibrinolytics amongst AIS patients and help to develop new and improved AIS therapeutics in future.
SN - 1868-4483
SN - 1868-601X
ER -