Dual roles of microglia in the pathological injury and repair of hemorrhagic cerebrovascular diseases

Abstract

Microglia are one of the most important immune cells in the central nervous system, which mainly play an immune surveillance role under normal conditions to maintain central nervous system homeostasis. In the early stages of hemorrhagic brain injury, microglia are activated to the classical phenotype (M1 type). At this time, microglia can promote the inflammatory response by secreting inflammatory cytokines and reactive oxygen species, thereby disrupting the blood–brain barrier. Consequently, this leads to neuronal cell necrosis, aggravates brain edema, and triggers secondary brain injury. However, in the later stages of hemorrhagic brain injury, microglia can switch from the M1 phenotype to the alternative activating M2 phenotype. This transition allows them to participate in the repair process of the nervous system after a brain hemorrhage. They achieve this by phagocytosing tissue debris, secreting anti-inflammatory cytokines, and releasing growth factors to suppress the overacting inflammatory response and promote angiogenesis. Therefore, this paper presents an account of cerebral hemorrhage and subarachnoid hemorrhage, with a primary focus on exploring the role of microglia in hemorrhagic cerebrovascular disease. The aim is to provide new perspectives for basic and clinical translational research in hemorrhagic cerebrovascular disease.