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.
Scientific Reports,
Journal Year:
2024,
Volume and Issue:
14(1)
Published: May 22, 2024
Abstract
Previous
reports
have
established
that
rESWT
fosters
angiogenesis,
yet
the
mechanism
by
which
promotes
cerebral
angiogenesis
remains
elusive.
stimulated
HUVECs
proliferation
as
evidenced
CCK-8
test,
with
an
optimal
dosage
of
2.0
Bar,
200
impulses,
and
2
Hz.
The
tube
formation
assay
revealed
peaked
at
36
h
post-rESWT
treatment,
concurrent
lowest
expression
level
Bach1,
detected
both
Western
blot
immunofluorescence.
Wnt3a,
β-catenin,
VEGF
also
h.
A
Bach1
overexpression
plasmid
was
transfected
into
HUVECs,
resulting
in
a
decreased
VEGF.
Upon
treatment
rESWT,
down-regulation
cells
reversed.
Wnt/β-catenin
inhibitor
DKK-1
utilized
to
suppress
Wnt3a
β-catenin
expression,
led
decrease
expression.
However,
could
restore
these
three
proteins,
even
presence
DKK-1.
Moreover,
OGD
model,
it
observed
inhibit
enhance
VEGFR-2
under
environment.
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.
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.
