Publication: Mechanisms of neuroinflammation and inflammatory mediators involved in brain injury following subarachnoid hemorrhage
Authors
Okada, Takeshi ; Suzuki, Hidenori
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Publisher
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/10.14670/HH-18-208
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info:eu-repo/semantics/article
Description
Abstract
Subarachnoid hemorrhage (SAH) is a
devastating cerebrovascular disorder. Neuro-
inflammation is a critical cause of brain injury following
SAH in both acute and chronic phases. While
accumulating evidence has shown that therapies
targeting neuroinflammation exerted beneficial effects in
experimental SAH, there is little clinical evidence. One
of the factors making neuroinflammation complicated is
that inflammatory signaling pathways and mediators act
as protective or detrimental responses at different
phases. In addition, biomarkers to detect neuro-
inflammation are little known in clinical settings. In this
review, first, we discuss how the inflammatory signaling
pathways contribute to brain injury and other secondary
pathophysiological changes in SAH. Damage-associated
molecular patterns arising from mechanical stress,
transient global cerebral ischemia, red blood cell
breakdown and delayed cerebral ischemia following
SAH trigger to activate pattern recognition receptors
(PRRs) such as Toll-like receptors, nucleotide-binding
oligomerization domain-like receptors, and receptors for
advanced glycation end products. Most of PRRs activate
common downstream signaling transcriptional factor
nuclear factor-κΒ and mitogen-activated protein kinases,
releasing pro-inflammatory mediators and cytokines.
Next, we focus on how pro-inflammatory substances
play a role during the course of SAH. Finally, we
highlight an important inducer of neuroinflammation,
matricellular protein (MCP). MCPs are a component of
extracellular matrix and exert beneficial and harmful
effects through binding to receptors, other matrix
proteins, growth factors, and cytokines. Treatment
targeting MCPs is being proved efficacious in pre-
clinical models for preventing brain injury including
neuroinflammation in SAH. In addition, MCPs may be a
candidate of biomarkers predicting brain injury
following SAH in clinical settings.
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Citation
Histology and Histopathology Vol. 35, nº7 (2020)
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