MicroRNAs regulate microglial polarization and influence the
neuroinflammatory response induced by intracerebral hemorrhage
- Demi Kong,
- Wei Zou
Abstract
Intracerebral hemorrhage is a common central nervous system disease
characterized by a high incidence, fatality and disablement rate.
Currently, there is no specific treatment available for this disease,
making it a major clinical challenge to overcome. Following an
intracerebral hemorrhage event, there is a leakage of blood components
from blood vessels into the brain. This leads to the activation of
microglia, which are specialized cells of the innate immune system.
Consequently, these cells release a plethora of inflammatory mediators.
Neuroinflammation in the adjacent vicinity of the hematoma and
throughout the entire brain can arise due to the interference caused by
microglia and inflammatory mediators. The extent of such inflammation is
intricately linked to secondary brain injury as well as the recovery of
brain function. Over the past few years, several investigations have
showcased the crucial function of microRNAs in governing disorders of
the central nervous system. This is specifically relevant when
considering the pathophysiological progression of intracerebral
hemorrhage and its associated neuroinflammatory cascade. By manipulating
the expression of microRNAs, these agents have the ability to impact the
behavior of immune cells and regulate the post-intracerebral hemorrhage
neuroinflammatory reaction. Consequently, this control could potentially
aid in mitigating the neurological functional deterioration arising from
secondary brain injury brought about by intracerebral hemorrhage.
Henceforth, the exploration of microRNAs as plausible molecular targets
to address intracerebral hemorrhage shall furnish novel concepts and
unveil untrodden avenues for its forthcoming treatment.