The Role of Complement C3a Receptor in Stroke

Document Type

Article

Abstract

© 2019, Springer Science+Business Media, LLC, part of Springer Nature. The complement system is a key regulator of the innate immune response against diseased tissue that functions across multiple organ systems. Dysregulation of complement contributes to the pathogenesis of a number of neurological diseases including stroke. The C3a anaphylatoxin, via its cognate C3a receptor (C3aR), mediates inflammation by promoting breakdown of the blood–brain barrier and the massive infiltration of leukocytes into ischemic brain in experimental stroke models. Studies utilizing complement deficient mice as well as pharmacologic C3aR antagonists have shown a reduction in tissue injury and mortality in murine stroke models. The development of tissue-specific C3aR knockout mice and more specific C3aR antagonists is warranted to facilitate our understanding of the role of the C3aR in brain ischemia with the ultimate goal of clinical translation of therapies targeting C3aR in stroke patients.

Keywords

C3a receptor, C3a receptor antagonist, Central nervous system, Complement cascade, Stroke

Publication Date

12-1-2019

Publication Title

NeuroMolecular Medicine

ISSN

15351084

E-ISSN

15591174

Volume

21

Issue

4

First Page

467

Last Page

473

PubMed ID

31102134

Digital Object Identifier (DOI)

10.1007/s12017-019-08545-7

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