Neural Regeneration Research,
Journal Year:
2024,
Volume and Issue:
20(8), P. 2199 - 2217
Published: July 29, 2024
Reperfusion
following
cerebral
ischemia
causes
both
structural
and
functional
damage
to
brain
tissue
could
aggravate
a
patient’s
condition;
this
phenomenon
is
known
as
ischemia-reperfusion
injury.
Current
studies
have
elucidated
the
neuroprotective
role
of
sirtuin
protein
family
(Sirtuins)
in
modulating
However,
potential
utilizing
it
novel
intervention
target
influence
prognosis
injury
requires
additional
exploration.
In
review,
origin
research
progress
Sirtuins
are
summarized,
suggesting
involvement
diverse
mechanisms
that
affect
injury,
including
inflammation,
oxidative
stress,
blood–brain
barrier
damage,
apoptosis,
pyroptosis,
autophagy.
The
therapeutic
avenues
related
may
improve
were
also
investigated
by
expression
affecting
representative
pathways,
such
nuclear
factor-kappa
B
signaling,
stress
mediated
adenosine
monophosphate-activated
kinase,
forkhead
box
O.
This
review
summarizes
endogenous
substances,
RNA
hormones,
drugs,
dietary
supplements,
emerging
therapies
regulate
expression.
reveals
regulating
mitigates
when
combined
with
other
risk
factors.
While
show
promise
for
treatment
most
recent
based
on
rodent
models
circadian
rhythms
distinct
from
those
humans,
potentially
influencing
efficacy
Sirtuins-targeting
drug
therapies.
Overall,
provides
new
insights
into
pathology
Journal of Neuroinflammation,
Journal Year:
2024,
Volume and Issue:
21(1)
Published: Feb. 6, 2024
Abstract
Stroke
is
a
clinical
syndrome
characterized
by
an
acute,
focal
neurological
deficit,
primarily
caused
the
occlusion
or
rupture
of
cerebral
blood
vessels.
In
stroke,
neuroinflammation
emerges
as
pivotal
event
contributing
to
neuronal
cell
death.
The
occurrence
and
progression
entail
intricate
processes,
prominently
featuring
mitochondrial
dysfunction
adaptive
responses.
Mitochondria,
double
membrane-bound
organelle
are
recognized
“energy
workshop”
body.
Brain
particularly
vulnerable
disturbances
due
its
high
energy
demands
from
mitochondria-related
production.
interplay
between
mitochondria
plays
significant
role
in
pathogenesis
stroke.
biological
pathological
consequences
resulting
stress
have
substantial
implications
for
function.
Mitochondrial
serves
mechanism
aimed
at
mitigating
induced
import
misfolded
proteins,
which
occurs
response
This
involves
reduction
protein
accumulation
overall
synthesis.
influence
on
state
stroke
underscored
capacity
interact
with
neuroinflammation.
impact
varies
according
severity.
Moderate
can
bolster
cellular
defenses,
enabling
cells
better
withstand
detrimental
stressors.
contrast,
sustained
excessive
detrimentally
affects
tissue
integrity.
relationship
depends
degree
present.
Understanding
instrumental
excavating
novel
treatment
review
aims
provide
evaluation
cross-talk
within
context
We
aim
reveal
how
environment
Frontiers in Molecular Neuroscience,
Journal Year:
2025,
Volume and Issue:
17
Published: Jan. 8, 2025
PANoptosis
is
a
novelly
defined
mode
of
programmed
cell
death
that
involves
the
activation
multiple
cellular
pathways,
including
pyroptosis,
apoptosis,
and
necroptosis,
triggering
robust
inflammatory
reactions.
Autophagy
crucial
process
maintains
homeostasis
protects
cells
from
various
stresses.
autophagy,
both
vital
players
in
intricate
pathological
progression
ischemic
stroke
(IS),
brain
ailment
governed
by
cascades,
have
garnered
attention
recent
years
for
their
potential
interplay.
While
mounting
evidence
hints
at
crosstalk
between
these
two
processes
IS,
underlying
mechanisms
remain
elusive.
Therefore,
this
review
delves
into
dissects
underpin
intersection
autophagy
devastating
condition.
In
conclusion,
IS
presents
promising
target
development
novel
therapies.
Understanding
interplay
pathways
offers
much-needed
insight
opens
possibility
new
therapeutic
strategies.
Journal of Cellular and Molecular Medicine,
Journal Year:
2025,
Volume and Issue:
29(4)
Published: Feb. 1, 2025
ABSTRACT
Cerebral
ischaemia–reperfusion
injury
(CIRI),
resulting
from
thrombolytic
therapy
for
ischaemic
stroke,
presents
a
considerable
challenge
during
postoperative
recovery.
Formononetin
(FMN)
has
shown
promise
in
the
prevention
and
treatment
of
neurological
diseases.
However,
its
specific
mechanism
ameliorating
CIRI
remains
uncertain.
Initially,
we
established
rat
model
to
evaluate
FMN's
therapeutic
potential
by
assessing
function,
infarct
area
pathological
changes.
Subsequently,
employed
metabolomics
technology
investigate
impact
on
metabolite
levels
brain
tissue
rats.
Based
findings,
validated
effects
nicotinate
nicotinamide
metabolism,
as
well
alanine,
aspartate
glutamate
along
with
influence
neuronal
repair.
Our
investigation
unveiled
that
FMN
intervention
significantly
diminished
Longa
score
asymmetry
rats,
constricted
ameliorated
alterations
tissue,
including
reduced
DCI
index
augmented
Nissl
body
count.
Metabolomics
analysis
indicated
exerted
regulatory
metabolism.
Following
intervention,
there
was
notable
increase
related
metabolites
such
(NAM),
L‐aspartic
acid
(L‐Asp),
fumaric
(FA),
gamma‐aminobutyric
(GABA)
L‐glutamic
(L‐Glu).
RT‐qPCR
Western
blot
outcomes
demonstrated
upregulated
gene
protein
expression
key
enzymes
adenylosuccinate
lyase
(ADSL)
glutamic
decarboxylase
(GAD)
involved
Moreover,
bolstered
SOD
activity,
MDA
ROS
TUNEL‐positive
expression.
Furthermore,
elevated
ATP
markedly
increased
Ki67‐positive
exhibits
alleviate
oxidative
stress
rats
enhancing
metabolism
consequently
reinstating
energy
conferring
neuroprotective
ameliorate
CIRI.
Autophagy,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 27, 2025
Mitochondrial
damage
and
dysfunction
are
hallmarks
of
neuronal
injury
during
cerebral
ischemia-reperfusion
(I/R).
Critical
mitochondrial
functions
including
energy
production
cell
signaling
perturbed
I/R,
often
exacerbating
contributing
to
secondary
injury.
The
integrity
the
proteome
is
essential
for
efficient
function.
proteostasis
mediated
by
cooperative
forces
mitophagy
intramitochondrial
proteolysis.
aim
this
study
was
elucidate
patterns
protein
dynamics
their
key
regulators
an
in
vitro
model
I/R
Utilizing
MitoTimer
reporter,
we
quantified
oxidation
turnover
injury,
highlighting
a
point
at
2
h
reoxygenation
aged/oxidized
turnover.
This
found
be
both
LONP1-dependent
proteolysis
PRKN/parkin-dependent
mitophagy.
Additionally,
proteostatic
response
mitochondria
influenced
fusion
fission
machinery.
Our
findings
highlight
involvement
Frontiers in Neuroscience,
Journal Year:
2025,
Volume and Issue:
18
Published: Jan. 7, 2025
Ischemic
stroke
is
a
major
cause
of
mortality
and
disability
worldwide.
Among
patients
with
ischemic
stroke,
the
primary
treatment
goal
to
reduce
acute
cerebral
injury
limit
infarct
size
in
timely
manner
by
ensuring
effective
reperfusion
through
administration
either
intravenous
thrombolysis
or
endovascular
therapy.
However,
can
induce
neuronal
death,
known
as
injury,
for
which
therapies
are
lacking.
Accumulating
data
supports
paradigm
whereby
ischemia/reperfusion
(I/R)
coupled
impaired
mitochondrial
function,
contributing
pathogenesis
stroke.
Herein,
we
review
recent
evidence
demonstrating
heterogeneous
response
following
I/R
placing
specific
focus
on
protein
modifications,
reactive
oxygen
species,
calcium
(Ca2+),
inflammation,
quality
control
under
experimental
conditions
using
animal
models.
The Journal of Cardiovascular Aging,
Journal Year:
2025,
Volume and Issue:
5(1)
Published: Jan. 22, 2025
With
the
increase
in
life
expectancy
globally,
challenge
of
dealing
with
aging
becomes
more
prominent.
Aging
is
a
risk
factor
for
several
diseases,
including
cardiovascular
disease.
Mitochondria,
which
have
long
been
studied
relation
to
aging,
play
crucial
role
maintaining
cellular
homeostasis.
However,
there
limitation
interorganellar
communication
as
organisms
age.
The
unfolded
protein
response
mitochondria
(UPRmt)
activated
during
stress
maintain
mitochondrial
homeostasis
and
prevent
accumulation
damaged
mitochondria.
This
involves
signaling
from
nucleus,
leading
transcriptional
changes.
In
context
heart,
this
review
explores
terms
function
morphology.
It
also
discusses
impact
UPRmt
on
cardiac
diseases
such
heart
failure,
acute
myocardial
infarction,
dilated
cardiomyopathy.
highlights
potential
mitochondria-endoplasmic
reticulum
contact
sites
(MERCs)
modulating
aging.
Finally,
it
provides
an
update
molecules
that
induce
activity,
potentially
benefiting
