Extracellular cold-inducible RNA-binding protein in CNS injury: molecular insights and therapeutic approaches
Dmitriy Lapin,
No information about this author
Archna Sharma,
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Ping Wang
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et al.
Journal of Neuroinflammation,
Journal Year:
2025,
Volume and Issue:
22(1)
Published: Jan. 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
Language: Английский
Role of efferocytosis in chronic pain —— From molecular perspective
Hu Zang,
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Xiaoyu Ji,
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Wenlong Yao
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et al.
Neurobiology of Disease,
Journal Year:
2025,
Volume and Issue:
207, P. 106857 - 106857
Published: Feb. 25, 2025
Language: Английский
Unveiling the neuroprotection effects of Volvalerenic acid A: Mitochondrial fusion induction via IDO1-mediated Stat3-Opa1 signaling pathway
Shanchun Ge,
No information about this author
Lei Wang,
No information about this author
Chang Jin
No information about this author
et al.
Phytomedicine,
Journal Year:
2024,
Volume and Issue:
129, P. 155555 - 155555
Published: March 20, 2024
Language: Английский
Notoginseng leaf triterpenes promotes angiogenesis by activating the Nrf2 pathway and AMPK/SIRT1-mediated PGC-1/ERα axis in ischemic stroke
Lei Wang,
No information about this author
Na Qin,
No information about this author
Shanchun Ge
No information about this author
et al.
Fitoterapia,
Journal Year:
2024,
Volume and Issue:
176, P. 106045 - 106045
Published: May 31, 2024
Language: Английский
Gut Microbiota and Tryptophan Metabolism in Pathogenesis of Ischemic Stroke: A Potential Role for Food Homologous Plants
Lei Wang,
No information about this author
Na Qin,
No information about this author
Liuliu Shi
No information about this author
et al.
Molecular Nutrition & Food Research,
Journal Year:
2024,
Volume and Issue:
68(23)
Published: Nov. 17, 2024
The
intestinal
flora
is
involved
in
the
maintenance
of
human
health
and
development
diseases,
closely
related
to
brain.
As
an
essential
amino
acid,
tryptophan
(TRP)
participates
a
variety
physiological
functions
body
affects
growth
body.
TRP
catabolites
produced
by
gut
microbiota
are
important
signaling
molecules
for
microbial
communities
host-microbe
interactions,
play
role
maintaining
disease
pathogenesis.
review
first
demonstrates
evidence
metabolism
stroke
relationship
between
metabolism.
Furthermore,
reveals
that
food
homologous
plants
(FHP)
bioactive
compounds
have
been
shown
regulate
various
metabolic
pathways
microbiota,
including
biosynthesis
valine,
leucine,
isoleucine,
vitamin
B6
most
notable
alteration
interaction
offers
plausible
explanation
bioactivities
FHP
treatment
ischemic
(IS).
This
enhances
comprehension
underlying
mechanisms
associated
with
bioactivity
on
IS.
Language: Английский
Efferocytosis: the resolution of inflammation in cardiovascular and cerebrovascular disease
Bingtao Zhang,
No information about this author
Yan Zou,
No information about this author
Z. Y. Yuan
No information about this author
et al.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: Nov. 26, 2024
Cardiovascular
and
cerebrovascular
diseases
have
surpassed
cancer
as
significant
global
health
challenges,
which
mainly
include
atherosclerosis,
myocardial
infarction,
hemorrhagic
stroke
ischemia
stroke.
The
inflammatory
response
immediately
following
these
profoundly
impacts
patient
prognosis
recovery.
Efficient
resolution
of
inflammation
is
crucial
not
only
for
halting
the
process
but
also
restoring
tissue
homeostasis.
Efferocytosis,
phagocytic
clearance
dying
cells
by
phagocytes,
especially
microglia
macrophages,
plays
a
critical
role
in
this
process.
Upon
injury,
phagocytes
are
recruited
to
site
damage
where
they
engulf
clear
through
efferocytosis.
Efferocytosis
suppresses
secretion
pro-inflammatory
cytokines,
stimulates
production
anti-inflammatory
modulates
phenotype
accelerates
inflammation,
promotes
repair.
It
involves
three
main
stages:
recognition,
engulfment,
degradation
cells.
Optimal
removal
apoptotic
cargo
requires
finely
tuned
machinery
associated
modifications.
Key
molecules
efferocytosis,
such
'Find-me
signals',
'Eat-me
'Don't
eat-me
been
shown
enhance
efferocytosis
cardiovascular
diseases.
Moreover,
various
additional
molecules,
pathways,
mitochondrial
metabolic
processes
identified
outcomes
via
diverse
experimental
models.
Impaired
can
lead
inflammation-associated
pathologies
prolonged
recovery
periods.
Therefore,
review
consolidates
current
understanding
mechanisms
its
application
diseases,
proposing
future
research
directions.
Language: Английский
Therapeutic implication of targeting mitochondrial drugs designed for efferocytosis dysfunction
Wan-Ting Liu,
No information about this author
Chao-Quan Li,
No information about this author
Ao-Ni Fu
No information about this author
et al.
Journal of drug targeting,
Journal Year:
2024,
Volume and Issue:
32(10), P. 1169 - 1185
Published: Aug. 5, 2024
Efferocytosis
refers
to
the
process
by
which
phagocytes
remove
apoptotic
cells
and
related
products.
It
is
essential
for
growth
development
of
body,
repair
damaged
or
inflamed
tissues,
balance
immune
system.
Damaged
efferocytosis
will
cause
a
variety
chronic
inflammation
system
diseases.
Many
studies
show
that
mediated
mitochondria.
Mitochondrial
metabolism,
mitochondrial
dynamics,
communication
between
mitochondria
other
organelles
can
all
affect
phagocytes'
clearance
cells.
Therefore,
targeting
modulate
phagocyte
an
anticipated
strategy
prevent
treat
inflammatory
diseases
autoimmune
In
this
review,
we
introduced
mechanism
pivoted
role
in
efferocytosis.
addition,
focused
on
therapeutic
implication
drugs
dysfunction.
Language: Английский
Ginsenoside Rb3 Promotes Opa1‐Mediated Regenerative Neurogenesis via Activating the Ido1 Pathway in Ischemic Stroke
Lei Wang,
No information about this author
Na Qin,
No information about this author
Shiman Gao
No information about this author
et al.
Phytotherapy Research,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Nov. 21, 2024
ABSTRACT
The
activation
of
neural
stem
cells
(NSCs)
residing
in
the
subventricular
zone
(SVZ)
and
dentate
gyrus
(DG)
has
been
shown
to
promote
restoration
damaged
brain
tissues.
Ginsenoside
Rb3
(Rb3)
is
a
bioactive
substance
known
for
its
pharmacological
properties
treating
neurological
disorders.
This
study
investigated
effects
on
regeneration
following
ischaemic
stroke
(IS)
underlying
mechanisms
involved.
Male
C57BL/6
mice
were
utilized
subjected
middle
cerebral
artery
occlusion/reperfusion
(MCAO/R).
Post‐ischemia,
was
administered
through
intraperitoneal
(i.p.)
injection
either
7
or
28
days.
promotion
regenerative
neurogenesis
detected
by
immunofluorescence
staining.
NSCs
pretreated
with
different
concentrations
24
h
before
oxygen–glucose
deprivation/reoxygenation
(OGD/R)
exposure.
Afterward,
staining
flow
cytometry
used
detect
migration
proliferation
OGD/R‐induced
NSCs.
Furthermore,
Adeno‐associated
virus
(AAV)
transduction
experiments,
siRNA
transfection
gene
knockout
targeted
metabolomics
analysis,
molecular
dynamics
simulation,
cellular
thermal
shift
assay
(CETSA),
drug
affinity
responsive
target
stability
(DARTS)
assays
explore
mechanism
IS.
promoted
Opa1‐mediated
proliferation.
Knockdown
Opa1
blunted
above‐promoting
both
brains
ischemia–reperfusion
(I/R)‐treated
OGD/R‐treated
Mechanistically,
metabolomics,
dynamics,
docking,
CETAS,
DARTS
experiments
showed
that
required
Ido1
served
as
direct
repair
I/R
injury.
Moreover,
studies
siRNA‐mediated
knockdown
KO
revealed
inhibition
attenuated
enhancing
effect
mitochondrial
fusion.
Our
provides
novel
evidence
promotes
an
Ido1/Opa1‐mediated
pathway
involving
interaction
between
Ido1,
leading
improved
long‐term
function.
These
results
indicate
other
fusion
promoters
could
be
potential
neurorestorative
strategy
Language: Английский