Extracellular cold-inducible RNA-binding protein in CNS injury: molecular insights and therapeutic approaches
Journal of Neuroinflammation,
Год журнала:
2025,
Номер
22(1)
Опубликована: Янв. 21, 2025
Abstract
Central
nervous
system
(CNS)
injuries,
such
as
ischemic
stroke
(IS),
intracerebral
hemorrhage
(ICH)
and
traumatic
brain
injury
(TBI),
are
a
significant
global
burden.
The
complex
pathophysiology
of
CNS
is
comprised
primary
secondary
injury.
Inflammatory
incited
by
damage-associated
molecular
patterns
(DAMPs)
which
signal
variety
resident
cells
infiltrating
immune
cells.
Extracellular
cold-inducible
RNA-binding
protein
(eCIRP)
DAMP
acts
through
multiple
non-immune
to
promote
inflammation.
Despite
the
well-established
role
eCIRP
in
systemic
sterile
inflammation,
its
less
elucidated.
Recent
literature
suggests
that
pleiotropic
inflammatory
mediator
also
being
evaluated
clinical
biomarker
indicate
prognosis
injuries.
This
review
provides
broad
overview
injury,
with
focus
on
immune-mediated
neuroinflammation.
We
then
what
known
about
mechanisms
both
non-CNS
cells,
identifying
opportunities
for
further
study.
explore
eCIRP’s
potential
prognostic
marker
severity
outcome.
Next,
we
provide
an
eCIRP-targeting
therapeutics
suggest
strategies
develop
these
agents
ameliorate
Finally,
emphasize
exploring
novel
mechanisms,
aside
from
neuroinflammation,
critical
therapeutic
target
Язык: Английский
Therapeutic Role of Microglia/Macrophage Polarization in Intracerebral Hemorrhage
Clinical and Translational Neuroscience,
Год журнала:
2025,
Номер
9(1), С. 4 - 4
Опубликована: Янв. 20, 2025
Intracerebral
hemorrhage
(ICH)
is
a
significant
health
problem
with
high
mortality
and
morbidity
rates,
partly
due
to
limited
treatment
options.
Hematoma
after
ICH
causes
neurological
deficits
the
mass
effect.
Hemorrhage
catalyzes
secondary
damage,
resulting
in
increased
poor
prognosis,
problems.
This
review
evaluates
role
of
immunotherapeutic
approaches
based
on
original
full-text
articles
pathophysiology
immunotherapy
ICH,
emphasis
modulation
microglia/macrophage
polarization
M2
subtype.
In
this
review,
we
concluded
that
injury
progression
complex
multifaceted.
Inflammation
plays
dominant
injuries.
Furthermore,
cells
involved
inflammatory
process
have
dual
roles
pro-inflammatory/destructive
anti-inflammatory/healing.
While
inflammation
makes
immune
system
therapeutic
target
them
can
modulate
Resident
microglia
(and
even
macrophages
migrating
from
peripheral
source)
are
important
targets
for
because
their
initiation
phase
shaping
immunity.
Although
clinical
results
remain
poor,
experimental
trial
data
seem
promising
deciphering
providing
Язык: Английский
Identification of AIF1 as a protein target of notoginsenosides in brain tissue of mice with intracerebral hemorrhage based on hapten immunoaffinity fishing technique
Journal of Ginseng Research,
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 1, 2025
Язык: Английский
A prospective cohort study on serum PINK1 as a biochemical marker in relation to poor neurological prognosis, stroke-associated pneumonia and early neurological deterioration after acute intracerebral hemorrhage
Clinica Chimica Acta,
Год журнала:
2025,
Номер
unknown, С. 120282 - 120282
Опубликована: Апрель 1, 2025
Язык: Английский
Activation of GPER1 alleviates white matter injury by promoting microglia M2 polarization through EGFR/Stat3 pathway in intracerebral hemorrhage mice
Journal of Stroke and Cerebrovascular Diseases,
Год журнала:
2025,
Номер
34(6), С. 108315 - 108315
Опубликована: Апрель 12, 2025
White
matter
injury
(WMI)
is
a
major
pathophysiological
process
after
intracerebral
hemorrhage
(ICH).
G
protein-coupled
estrogen
receptor
1
(GPER1)
has
been
validated
to
exert
crucial
role
in
regulating
neuroinflammation
and
microglia
polarization.
Our
previous
report
reveals
activation
of
GPER1
improves
the
neurological
deficits
ICH
via
inhibition
A1
astrocytes.
However,
on
protection
WMI
modulation
polarization
remains
unclear.
In
present
study,
mice
model
was
induced
by
autologous
whole
blood
injection
vitro
established
treatment
BV2
cells
with
FeSO4.
Mice
were
treated
agonist
G1,
antagonist
G15
or
EGFR
inhibitor
AG1478.
Besides,
conditional
medium
used
intervene
MO3.13
oligodendrocytes.
Immunostaining,
immunoblots,
transmission
electron
microscope
PI
staining
determine
WMI,
potential
molecular
mechanism
ICH,
respectively.
data
showed
G1
ameliorated
day
3
ICH.
reduced
release
IL-1β,
TNF-α
increased
produce
IL-4,
IL-10
as
well
shifting
from
proinflammatory
M1
anti-inflammatory
M2
phenotype
vivo
vitro.
Meanwhile,
alleviated
oligodendrocytes
death
mitigating
modulating
Mechanistic
study
demonstrated
EGFR/Stat3
signaling
pathway
involved
Collectively,
our
findings
through
pathway.
Язык: Английский