TY - JOUR
T1 - Thromboinflammation in Brain Ischemia
T2 - Recent Updates and Future Perspectives
AU - De Meyer, Simon F
AU - Langhauser, Friederike
AU - Haupeltshofer, Steffen
AU - Kleinschnitz, Christoph
AU - Casas, Ana I
N1 - Funding Information:
This project has received funding from the European Union’s Horizon 2020 research and innovation program under grant agreement No 777111 (REPO-TRIAL). This reflects only the author’s view, and the European Commission is not responsible for any use that may be made of the information it contains. Dr Casas was supported by the Deutsche Forschungsgemeinschaft (DFG) Walter Benjamin Program (ref. DFG CA 2642/1-1) and Förderprogramm der Corona-Stiftung im Stifterverband. Dr Kleinschnitz, Langhauser received funding from the DFG Forschungsgruppe FOR 2879 (ref. 428778684). Dr De Meyer received funding from Fonds voor Wetenschappelijk Onderzoek–Vlaanderen (FWO) (research grants G0A8613, G078517, 1509216 N and G0E7620N), the Katholieke Universiteit Leuven (OT/14/099, ISP/14/02L2 and PDM/20/147), the Queen Elisabeth Medical Foundation and by the European Union’s Horizon 2020 Research and Innovation Program INSIST under grant agreement No. 777072.
Publisher Copyright:
© 2022 Lippincott Williams and Wilkins. All rights reserved.
PY - 2022/5
Y1 - 2022/5
N2 - Despite decades of promising preclinical validation and clinical translation, ischemic stroke still remains as one of the leading causes of death and disability worldwide. Within its complex pathophysiological signatures, thrombosis and inflammation, that is, thromboinflammation, are highly interconnected processes leading to cerebral vessel occlusion, inflammatory responses, and severe neuronal damage following the ischemic event. Hence, we here review the most recent updates on thromboinflammatory-dependent mediators relevant after stroke focusing on recent discoveries on platelet modulation, a potential regulation of the innate and adaptive immune system in thromboinflammation, utterly providing a thorough up-to-date overview of all therapeutic approaches currently undergoing clinical trial.
AB - Despite decades of promising preclinical validation and clinical translation, ischemic stroke still remains as one of the leading causes of death and disability worldwide. Within its complex pathophysiological signatures, thrombosis and inflammation, that is, thromboinflammation, are highly interconnected processes leading to cerebral vessel occlusion, inflammatory responses, and severe neuronal damage following the ischemic event. Hence, we here review the most recent updates on thromboinflammatory-dependent mediators relevant after stroke focusing on recent discoveries on platelet modulation, a potential regulation of the innate and adaptive immune system in thromboinflammation, utterly providing a thorough up-to-date overview of all therapeutic approaches currently undergoing clinical trial.
KW - ARTERIAL THROMBOSIS
KW - B-CELLS
KW - FOCAL CEREBRAL-ISCHEMIA
KW - GLYCOPROTEIN-IIB/IIIA
KW - LIMIT CNS INFLAMMATION
KW - MAST-CELLS
KW - PROTECTS MICE
KW - REGULATORY T-CELLS
KW - THROMBO-INFLAMMATION
KW - VON-WILLEBRAND-FACTOR
KW - inflammation
KW - ischemic stroke
KW - microglia
KW - thromboinflammation
KW - thrombosis
U2 - 10.1161/STROKEAHA.122.038733
DO - 10.1161/STROKEAHA.122.038733
M3 - (Systematic) Review article
C2 - 35360931
SN - 0039-2499
VL - 53
SP - 1487
EP - 1499
JO - Stroke
JF - Stroke
IS - 5
ER -