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The Complex Role of the Complement C3a Receptor (C3aR) in Cerebral Injury and Recovery Following Ischemic Stroke
Naseem Akhter1, Ateeq Lambay1, Reema Almotairi2
1Department of Translational Neuroscience, Barrow Neurological Institute, Phoenix, AZ 85013, USA.
Cells
|September 26, 2025
Summary
Targeting the Complement C3a Receptor (C3aR) requires careful timing after cerebral ischemia. Blocking C3aR acutely reduces brain injury, while later modulation promotes tissue repair and recovery.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Cerebral ischemia triggers complement activation, involving the C3a Receptor (C3aR) and its ligand C3a.
- C3aR, a G-protein-coupled receptor, exhibits time-dependent roles in brain injury and repair following ischemic events.
Purpose of the Study:
- To elucidate the multifaceted, time-dependent roles of C3aR in cerebral ischemia.
- To explore therapeutic strategies targeting the C3a/C3aR axis for optimizing outcomes after brain injury.
Main Methods:
- Review of existing literature on C3aR function in cerebral ischemia.
- Analysis of C3aR's impact across acute, subacute, and chronic phases of brain injury.
Main Results:
- Acute C3aR activation exacerbates injury by increasing inflammation, BBB permeability, and edema.
- Subacute C3aR activity can worsen secondary injury but also aids debris clearance and cell survival.
- Chronic C3aR activity may prolong neuroinflammation, yet controlled signaling promotes repair pathways.
Conclusions:
- Therapeutic targeting of C3aR necessitates a time-dependent strategy.
- Blocking C3aR in the acute phase mitigates initial damage.
- Modulating C3aR in later phases promotes neuroprotection and functional recovery.
