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.
Biomedical Papers,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Dec. 17, 2024
Traumatic
brain
injury
(TBI)
has
long-term
consequences,
including
neurodegenerative
disease
risk.
Current
diagnostic
tools
are
limited
in
detecting
subtle
damage.
This
review
explores
emerging
biomarkers
for
TBI,
those
related
to
neuronal
injury,
inflammation,
EVs,
and
ncRNAs,
evaluating
their
potential
predict
clinical
outcomes
like
mortality,
recovery,
cognitive
impairment.
It
addresses
challenges
opportunities
implementing
practice,
aiming
improve
TBI
diagnosis,
prognosis,
treatment.
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.
