Reviews in the Neurosciences,
Год журнала:
2024,
Номер
unknown
Опубликована: Дек. 16, 2024
Abstract
Stroke
is
a
severe
neurological
disease
and
major
worldwide
issue,
mostly
manifesting
as
ischemic
stroke
(IS).
In
order
to
create
effective
treatments
for
IS,
it
imperative
fully
understand
the
underlying
pathologies,
existing
therapeutic
choices
are
inadequate.
Recent
investigations
have
shown
complex
relationships
between
several
programmed
cell
death
(PCD)
pathways,
including
necroptosis,
ferroptosis,
pyroptosis,
their
correlation
with
immune
responses
during
IS.
However,
this
relationship
still
unclear.
To
address
gap,
review
study
explored
cellular
interactions
in
microenvironment
of
Then,
validate
prior
findings
uncover
biomarkers,
investigated
bioinformatics
studies.
Several
nuclear
factor
kappa-light-chain-enhancer
activated
B
cells
(NF-κB),
Toll-like
receptor
4
(TLR4),
receptor-interacting
protein
kinase
(RIPK),
were
involved
PCD-immune
interactions.
The
studies
reported
key
biomarkers
such
glutathione
peroxidase
(GPX4),
NOD-like
family
pyrin
domain
containing
3
(NLRP3),
gasdermin
D
(GSDMD),
TLR4,
which
important
implications
cuproptosis,
necroptosis
respectively.
These
associated
PCD
mechanisms
oxidative
stress
inflammatory
reactions.
infiltration
analysis
consistently
revealed
significant
pathways
detrimental
cells,
neutrophils
γδ
T
cells.
Conversely,
M2
macrophages
helper
showed
protective
effects.
conclusion,
considering
intricate
network
emphasized
necessity
paradigm
shift
approaches
injuries
that
related
network.
International Journal of Molecular Sciences,
Год журнала:
2025,
Номер
26(3), С. 868 - 868
Опубликована: Янв. 21, 2025
Cardiometabolic
and
cardiovascular
diseases
(CVDs)
remain
the
leading
cause
of
death
worldwide,
with
well-established
risk
factors
such
as
smoking,
obesity,
diabetes
contributing
to
plaque
formation
chronic
inflammation.
However,
emerging
evidence
suggests
that
immune
system
plays
a
more
significant
role
in
development
progression
CVD
than
previously
thought.
Specifically,
finely
tuned
regulation
lymphocyte
subsets
governs
post-injury
inflammation
tissue
damage
resolution
orchestrates
functions
activation
endothelial
cells,
cardiomyocytes,
fibroblasts
CVD-associated
lesions
(e.g.,
atherosclerotic
plaques).
A
deeper
understanding
system’s
involvement
will
provide
new
insights
into
disease
biology
uncover
novel
therapeutic
targets
aimed
at
re-establishing
homeostasis.
In
this
review,
we
summarize
current
state
knowledge
on
distribution
CVD,
including
atherosclerosis,
diabetes,
hypertension,
myocardial
infarction,
stroke.
Journal of Inflammation Research,
Год журнала:
2025,
Номер
Volume 18, С. 3055 - 3066
Опубликована: Март 1, 2025
Ischemic
stroke
is
characterized
by
a
high
incidence
and
elevated
mortality.
events
trigger
neuroinflammation,
leading
to
severe
brain
edema
neuronal
necrosis.
Microglia
are
the
primary
mediators
of
neuroinflammation.
Inhibition
M1
microglia
effectively
alleviate
damage
in
mild
stroke.
TPT-260
minimally
cytotoxic,
small
molecule
chaperone
retromer
complex,
which
mediates
recycling
trafficking
membrane
protein
receptors.
This
study
explores
therapeutic
effects
related
mechanisms
model
mice
from
an
anti-inflammatory
perspective,
aiming
evaluate
efficacy
mechanism
treating
In
this
study,
middle
cerebral
artery
occlusion
(MCAO)
animal
was
established
simulate
ischemic
Primary
were
cultured
for
lipopolysaccharides
treatment
construct
microglia.
Both
animals
cells
treated
with
TPT-260.
Nuclear
factor-κB
(NF-κB)
nuclear
translocation
expression
downstream
pro-inflammatory
factors
Interleukin
1β
(IL-1β)
Tumor
necrosis
factor-α
(TNF-α)
determined.
vivo
results
revealed
that
significantly
reduced
infarct
area
inflammation
as
well
improved
neurological
function
mice.
The
potential
involved
marked
inhibition
lipopolysaccharides-induced
suppressing
NF-κB
attenuating
IL-1β
TNF-α.
Moreover,
inhibited
NOD-like
receptor
3
inflammasome
formation,
thereby
decreasing
release
mature
alleviating
attenuated
via
repression
signaling,
thus
preventing
neuroinflammation
injuries
Frontiers in Aging Neuroscience,
Год журнала:
2025,
Номер
17
Опубликована: Апрель 4, 2025
Cognitive
dysfunction
is
a
common
and
debilitating
complication
following
ischemic
stroke,
significantly
impairing
the
quality
of
life
patients.
In
recent
years,
aerobic
exercise
has
emerged
as
promising
non-pharmacological
intervention
to
mitigate
post-stroke
cognitive
impairment
(PSCI).
This
review
synthesizes
current
evidence
on
efficacy
mechanisms
in
enhancing
recovery
after
stroke.
Key
include
improved
cerebral
hemodynamics
through
enhanced
blood
flow
(CBF),
promotion
neuroplasticity
via
brain-derived
neurotrophic
factor
(BDNF)-mediated
pathways,
suppression
neuroinflammation
(e.g.,
NLRP3
inflammasome
inhibition),
attenuation
oxidative
stress.
Preclinical
clinical
studies
demonstrate
that
modalities
such
gait
training,
cycling,
aquatic
therapy
enhance
domains
including
memory,
executive
function,
attention,
with
optimal
benefits
observed
at
moderate-to-high
intensity
frequency
≥3
sessions
per
week.
Despite
robust
evidence,
challenges
remain
standardizing
protocols
addressing
individual
variability
treatment
response.
Future
research
should
prioritize
large-scale
randomized
controlled
trials
validate
long-term
identify
biomarkers
for
personalized
rehabilitation
strategies.
underscores
imperative
integrate
into
paradigms,
offering
dual
therapeutic
approach
improve
both
physical
outcomes.
Frontiers in Bioscience-Landmark,
Год журнала:
2025,
Номер
30(5)
Опубликована: Апрель 29, 2025
Background:
Ischemic
stroke
triggers
inflammatory
responses
that
lead
to
neuronal
damage,
with
microglial
polarization
significantly
influencing
post-stroke
inflammation.
This
study
explores
the
role
of
Fc
gamma
receptor
Ia
(FCGR1A)
in
and
its
regulatory
mechanisms
ischemic
stroke.
Methods:
Differentially
expressed
genes
(DEGs)
associated
were
identified
using
GSE58294
dataset.
Hub
found
by
analyzing
protein–protein
interaction
(PPI)
networks.
BV2
microglia
subjected
oxygen–glucose
deprivation/reoxygenation
(OGD/R)
mimic
conditions
vitro,
FCGR1A
marker
levels
assessed.
Besides,
cells
stimulated
lipopolysaccharide
(LPS)
interferon-gamma
(IFN-γ)
induce
M1
polarization,
effects
overexpression
knockdown
on
cytokine
production
evaluated.
The
function
AMP-activated
protein
kinase
(AMPK)-mTOR
pathway
regulating
was
further
investigated
mTOR
inhibitor
rapamycin
(RAP).
Results:
From
327
DEGs
identified,
chosen
as
a
hub
gene.
OGD/R
treatment
produced
time-dependent
rise
FCGR1A,
induction
brown
adipocytes
1
(Iba1),
interleukin
6
(IL-6)
expression,
indicating
enhanced
induced
proinflammatory
response
promoted
whereas
reduced
inflammation
shifted
toward
an
anti-inflammatory
M2
phenotype.
Inhibition
RAP,
combined
knockdown,
AMPK
activation
shift
Conclusion:
modulates
affecting
AMPK–mTOR
signaling
conditions.
Targeting
related
pathways
could
offer
new
therapeutic
strategies
lessen
facilitate
healing
process
after
