Abstract
Aneurysms and vascular malformations of the brain represent an important source of intracranial hemorrhage and subsequent mortality and morbidity. We are only beginning to discern the involvement of microglia, the resident immune cell of the central nervous system, in these pathologies and their outcomes. Recent evidence suggests that activated proinflammatory microglia are implicated in the expansion of brain injury following subarachnoid hemorrhage (SAH) in both the acute and chronic phases, being also a main actor in vasospasm, considerably the most severe complication of SAH. On the other hand, anti-inflammatory microglia may be involved in the resolution of cerebral injury and hemorrhage. These immune cells have also been observed in high numbers in brain arteriovenous malformations (bAVM) and cerebral cavernomas (CCM), although their roles in these lesions are currently incompletely ascertained. The following review aims to shed a light on the most significant findings related to microglia and their roles in intracranial aneurysms and vascular malformations, as well as possibly establish the course for future research.
Highlights
Intracranial aneurysms are pathological dilations of arteries and represent the point of minimal resistance of their parent vessel, as well as the greatest source of non-traumatic subarachnoid hemorrhage (SAH)
Brain arteriovenous malformations and cerebral cavernous malformations (CCM) are predominantly congenital lesions of the intracranial vasculature, with the first possessing high blood flow, and the latter low to minimal internal flow. Both possess a predisposition for rupture and debilitating cerebral hemorrhage based on their location, bAVMs being especially prone to this complication
Duduki et al found that the lack of intracellular adapter Kindlin3, which within the central nervous system (CNS) is exclusively expressed by microglia, leads to increased microglial contractility, dysregulation of the ERK pathway, overexpression of transforming growth factor-beta 1 (TGFβ1), and malformed vasculature within the retina [28]
Summary
Intracranial aneurysms are pathological dilations of arteries and represent the point of minimal resistance of their parent vessel, as well as the greatest source of non-traumatic subarachnoid hemorrhage (SAH). Brain arteriovenous malformations (bAVM) and cerebral cavernous malformations (CCM) are predominantly congenital lesions of the intracranial vasculature, with the first possessing high blood flow, and the latter low to minimal internal flow Both possess a predisposition for rupture and debilitating cerebral hemorrhage based on their location, bAVMs being especially prone to this complication. Other sources of origin have been proposed, such as the neuroectodermal or mesodermal precursor cells [21] They are crucial in maintaining the homeostasis of the central nervous system (CNS) microenvironment, possessing the capacity to shift their function toward either the pro- (M1) or anti-inflammatory (M2) phenotype to protect the brain . The paragraphs may provide a meaningful insight on the lesser-known aspects of brain inflammation and immunologic response correlated with these pathologies
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