Expert Opinion on Therapeutic Targets,
Journal Year:
2024,
Volume and Issue:
unknown, P. 1 - 27
Published: Dec. 23, 2024
Introduction
Ischemic
stroke
(IS),
a
major
cause
of
mortality
and
disability
worldwide,
remains
significant
healthcare
challenge
due
to
limited
therapeutic
options.
Ferroptosis,
distinct
iron-dependent
form
regulated
cell
death
characterized
by
lipid
peroxidation
oxidative
stress,
has
emerged
as
crucial
mechanism
in
IS
pathophysiology.
This
review
explores
the
role
ferroptosis
its
potential
for
driving
innovative
strategies.
Abstract
Ferroptosis
is
a
newly
discovered
form
of
programmed
cell
death
that
non‐caspase‐dependent
and
characterized
by
the
production
lethal
levels
iron‐dependent
lipid
reactive
oxygen
species
(ROS).
In
recent
years,
ferroptosis
has
attracted
great
interest
in
field
cerebral
infarction
because
it
differs
morphologically,
physiologically,
genetically
from
other
forms
such
as
necrosis,
apoptosis,
autophagy,
pyroptosis.
addition,
ROS
considered
to
be
an
important
prognostic
factor
for
ischemic
stroke,
making
promising
target
stroke
treatment.
This
paper
summarizes
induction
defense
mechanisms
associated
with
ferroptosis,
explores
potential
treatment
strategies
order
lay
groundwork
development
new
neuroprotective
drugs.
ACS Omega,
Journal Year:
2024,
Volume and Issue:
unknown
Published: March 10, 2024
The
protective
role
of
hydrogen
sulfide
against
cerebral
ischemia-reperfusion
injury
involves
the
inhibition
RhoA-/Rho-associated
coiled-coil
kinase
(ROCK)
pathway.
However,
specific
mechanism
remains
elusive.
This
study
investigates
impact
on
RhoA
phosphorylation
at
serine
188
(Ser188)
in
vivo,
aiming
to
test
hypothesis
that
exerts
neuroprotection
by
enhancing
Ser188,
subsequently
inhibiting
RhoA/ROCK
Recombinant
RhoAwild-pEGFP-N1
and
RhoAS188A-pEGFP-N1
plasmids
were
constructed
administered
via
stereotaxic
injection
into
rat
hippocampus.
A
global
model
was
induced
bilateral
carotid
artery
ligation
elucidate
neuroprotective
mechanisms
sulfide.
Both
expressed
RhoAwild
RhoAS188A
proteins,
respectively,
hippocampal
tissues,
alongside
intrinsic
protein.
Systemic
administration
exogenous
donor
sodium
hydrosulfide
led
an
increase
Ser188
transfected
protein
within
this
effect
not
observed
tissues
with
RhoAS188A.
Sodium
hydrosulfide-mediated
correlated
decreased
ROCK2
activity
tissues.
Furthermore,
reduced
ischemia-reperfusion-induced
neuronal
damage
apoptosis
RhoAwild.
attenuated
rats
These
findings
suggest
ischemia/reperfusion
increased
Ser188.
Promoting
may
represent
a
potential
therapeutic
target
for
ischemic
stroke.
OncoTargets and Therapy,
Journal Year:
2023,
Volume and Issue:
Volume 16, P. 983 - 994
Published: Nov. 1, 2023
Ligustilide
(LIG)
and
n-butylphthalide
(NBP)
have
neuroprotective
effects
in
cerebral
ischemia;
however,
their
roles
gliomas
are
not
well-known.This
study
aimed
to
explore
the
anti-glioma
of
LIG
NBP
individually
synergistic
temozolomide
(TMZ)
via
PI3K/Akt
Signaling
Pathway.Cytotoxicity
alone
combination
with
TMZ
U251
cells
was
determined
using
CCk-8.
The
effect
compounds
or
on
cell
migration
detected
wound
healing
assay,
invasion
evaluated
by
transwell
assays,
respectively.
Cell
apoptosis
quantified
flow
cytometry
changed
expressions
proteins
were
Western
blotting.The
results
showed
that
significantly
inhibited
growth
at
concentrations
4-10
µg/mL
1.5-6
a
dose-dependent
manner
(p<0.05,
p<0.01).
20
concentration
range
0.5-6
µg/mlachieved
towardsU251
cells.
NBP,
TMZ,
markedly
(p<
0.001)
enhanced
0.05).
0.001).
blot
analysis
LIG,
combination,
decreased
expression
Bcl-2,
p-PI3K,
p-Akt,
increased
Bax.Both
exert
own
through
pathway
enhance
TMZ-mediated
efficiency
same
pathway.
Deleted Journal,
Journal Year:
2024,
Volume and Issue:
unknown, P. 1 - 14
Published: Nov. 10, 2024
Ferroptosis,
a
regulated
form
of
cell
death
characterized
by
iron-dependent
lipid
peroxidation,
has
emerged
as
key
contributor
to
neuronal
damage
in
various
types
brain
injury,
including
traumatic
injury
(TBI)
and
ischemic
caused
brian
ischemia
(BI).
This
review
summarizes
the
underlying
mechanisms
ferroptosis
injuries
highlights
its
role
exacerbating
loss,
inflammation,
secondary
damage.
After
TBI,
release
free
iron
oxidative
stress
after
triggers
ferroptosis,
contributing
long-term
neurological
deficits.
Similarly,
BI,
is
initiated
accumulation
reactive
oxygen
species
(ROS)
mitochondrial
dysfunction
during
reperfusion,
further
amplifying
The
current
provides
comprehensive
overview
interplay
between
with
an
emphasis
on
potential
targeting
improve
recovery
outcomes
patients.
Future
research
directions
include
development
novel
inhibitors
integration
ferroptosis-targeting
strategies
existing
treatment
modalities.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(23), P. 12541 - 12541
Published: Nov. 22, 2024
Doxorubicin
(DOX),
an
anticancer
drug,
is
used
to
treat
several
types
of
tumors,
but
it
has
detrimental
side
effects
that
restrict
its
therapeutic
efficacy.
One
the
iron-dependent
form
ferroptosis,
which
characterized
by
elevated
ROS
production
and
iron
overload.
Research Square (Research Square),
Journal Year:
2024,
Volume and Issue:
unknown
Published: Dec. 19, 2024
Abstract
Synchronized
neurogenesis
and
angiogenesis
after
stroke
have
been
well
documented,
inducing
neurovascular
remodeling
may
provide
a
promising
strategy
to
promote
tissue
repair
functional
recovery.
Dl-3-n-butylphthalide
(NBP)
was
reported
exert
potent
angiogenic
activity
in
rodent
models
of
stroke.
However,
little
is
currently
known
regarding
the
effects
mechanisms
NBP
on
ischemic
This
study
determine
whether
how
promoted
cerebral
injury.
Adult
C57BL/6
mice,
subjected
occlusion
distal
branches
middle
artery
(dMCAO),
were
treated
with
NBP.
The
efficacy
assessed
using
neurologic
deficits
infarct
volume.
Immunofluorescent
staining
applied
evaluate
neurogenesis.
regulation
Wnt/β-catenin
signaling
pathway
neurotrophic
factors
detected
by
western
blotting
qRT-PCR.
Administration
reduced
volume
ameliorated
neurological
proliferation
NSCs
SVZ,
migration
neuroblasts
along
corpus
callosum,
differentiation
towards
neurons
peri-infarct
zone,
resulting
restored
neural
function.
Moreover,
we
revealed
that
NBP-induced
associated
activation
pathway,
which
reversed
DKK1.
In
addition,
increased
production
VEGF
BDNF.
Our
data
unveiled
potentials
recovery
stroke,
dependent
production.
Thus,
be
candidate
for
delayed
treatment
