The Role of Complement C3a Receptor in Stroke
Abstract
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.
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Complement factor C3 is markedly up-regulated in cEDS cells.
“Of note is also the marked up-regulation of the complement factor C3 belonging to a complex network of plasma and membrane proteins involved in the innate immunity [74].”
From Cellular and Molecular Mechanisms in the Pathogenesis of Classical, Vascular, and Hypermobile Ehlers‒Danlos Syndromes (2019) · cites this paper as [74]
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- Authors
- Ahmad, S., Bhatia, K., Kindelin, A., & Ducruet, A. F.
- Affiliations
- Barrow Neurological Institute (US)
- Corresponding author
- Ahmad, Saif
- Ducruet, Andrew F.
- Venue
- NeuroMolecular Medicine
- Published
- 2019-05-17
- Volume
- 21
- Issue
- 4
- Pages
- 467-473
- ISSN
- 1535-1084 (ISSN-L)
- 1559-1174
- OpenAlex
- W2945227497
- Cited by
- 21
- References
- 69
- Citations by year
- 2025: 5 · 2024: 4 · 2023: 1 · 2022: 3 · 2021: 5 · 2020: 2 · 2019: 1
- FWCI
- 0.24
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- NeuroMolecular Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Barrow Neurological Foundation (start up, trainee grant)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Complement system in diseases
- Health Sciences › Medicine › Epidemiology › Acute Ischemic Stroke Management
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- C3a receptor, C3a anaphylatoxin, stroke, ischemic brain injury, blood-brain barrier disruption, leukocyte infiltration, complement dysregulation, neuroinflammation, innate immunity
- MeSH terms
- Animals, Arginine, Benzhydryl Compounds, Blood-Brain Barrier, Complement Activation, Disease Models, Animal, Humans, Immunity, Innate, Receptors, Complement, Neuroimmunomodulation, Complement C3a, Mice, Knockout, Neuroprotective Agents, Stroke, Complement Inactivating Agents, Mice, Translational Research, Biomedical
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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