After a cerebral hemorrhage (intracerebral, subarachnoid, and intraventricular), extravasated blood contributes to both initial brain injury, via physical disruption and mass effect, and secondary injury, through the release of potentially neurotoxic and pro-inflammatory factors such as hemoglobin, iron, and peroxiredoxin-2. Erythrocytes are a major blood component and are a source of such damaging factors. Erythrolysis after cerebral hemorrhage releases potential neurotoxins, contributing to brain injury and edema. Alternatively, erythrocyte phagocytosis via microglia or macrophages may limit the spill of neurotoxins therefore limiting subsequent brain injury. The aim of this review is to discuss the process of phagocytosis of erythrocytes by microglia or macrophages after cerebral hemorrhage, the effect of erythrolysis on brain injury, novel mechanisms of erythrocyte and phagocyte egress from the brain, and exciting new targets in this pathway to attenuate brain injury. Understanding the fate of erythrocytes after cerebral hemorrhage may uncover additional potential interventions for clinical translational research.
Keywords: Cerebral hemorrhage; Complement; Erythrocytes; Erythrolysis; Macrophages; Microglia; Phagocytosis.
© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.