Role of gC1qR as a modulator of endothelial cell permeability and contributor to post-stroke inflammation and edema formation.

Autor:	Delgardo M; Department of Neurological Surgery, Columbia University Irving Medical Center, New York, NY, United States., Tang AJ; Department of Neurological Surgery, Columbia University Irving Medical Center, New York, NY, United States., Tudor T; Department of Neurological Surgery, Columbia University Irving Medical Center, New York, NY, United States., Pascual-Leone A; Department of Neurological Surgery, Columbia University Irving Medical Center, New York, NY, United States., Connolly ES Jr; Department of Neurological Surgery, Columbia University Irving Medical Center, New York, NY, United States.
Jazyk:	angličtina
Zdroj:	Frontiers in cellular neuroscience [Front Cell Neurosci] 2023 Jun 13; Vol. 17, pp. 1123365. Date of Electronic Publication: 2023 Jun 13 (Print Publication: 2023).
DOI:	10.3389/fncel.2023.1123365
Abstrakt:	Ischemic stroke is a leading cause of death and disability worldwide. A serious risk of acute ischemic stroke (AIS) arises after the stroke event, due to inflammation and edema formation. Inflammation and edema in the brain are mediated by bradykinin, the formation of which is dependent upon a multi-ligand receptor protein called gC1qR. There are currently no preventive treatments for the secondary damage of AIS produced by inflammation and edema. This review aims to summarize recent research regarding the role of gC1qR in bradykinin formation, its role in inflammation and edema following ischemic injury, and potential therapeutic approaches to preventing post-stroke inflammation and edema formation. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2023 Delgardo, Tang, Tudor, Pascual-Leone and Connolly.)
Databáze:	MEDLINE
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