Authorea (Authorea),
Journal Year:
2023,
Volume and Issue:
unknown
Published: June 8, 2023
Ferroptosis
is
a
new
non-apoptotic
form
of
regulatory
cell
death,
which
characterized
by
intracellular
iron
overload
and
excessive
accumulation
lipid
peroxides
reactive
oxygen
species
(ROS).
closely
related
to
iron,
amino
acid,
metabolism
disorders.
increasingly
recognized
as
an
important
process
mediating
the
pathogenesis
progression
acute
ischemic
stroke,
it
can
be
involved
in
influencing
stroke
risk
factors
atherosclerosis,
atrial
fibrillation,
hypertension,
diabetes
mellitus,
obstructive
sleep
apnea.
Therefore,
understanding
mechanisms
ferroptosis
regulation
different
diseases
may
have
significant
implications
for
preventive
treatment
improvement
prognosis
patients
with
stroke.
This
article
reviews
not
only
specific
development
but
also
relevant
associations
between
ferroptosis,
describes
current
limitations
future
directions
its
factors.
Frontiers in Pharmacology,
Journal Year:
2025,
Volume and Issue:
16
Published: Feb. 24, 2025
Atherosclerosis
(AS)-related
cardiovascular
disease
and
depression
are
often
comorbid,
with
patients
facing
an
increased
risk
of
depression,
which
worsens
AS.
Both
diseases
characterized
by
oxidative
stress
lipid
metabolism
disorders.
Ferroptosis,
a
form
cell
death
iron
overload
harmful
peroxide
accumulation,
is
found
in
various
diseases,
including
AS
depression.
Consistent
the
deposition
peroxidation
(LPO)
that
characterize
ferroptosis
mechanism,
disturbances
also
crucial
pathogenic
mechanisms
The
comorbid
complex,
posing
challenges
for
clinical
treatment.
Chinese
herbs
hold
significant
potential
owing
to
their
multi-target
pharmacological
effects.
Therefore,
this
review
aims
investigate
overload,
LPO,
across
types,
shared
pathogenesis
ferroptosis,
research
on
herbal
medicine
targeting
treatment
anti-AS
co-depression.
This
provides
comprehensive
understanding
co-depression
from
perspective
ferroptosis.
Cellular Signalling,
Journal Year:
2025,
Volume and Issue:
unknown, P. 111728 - 111728
Published: March 1, 2025
Ischemic
stroke,
a
neurological
condition
with
complicated
etiology
that
is
accompanied
by
severe
inflammation
and
oxidative
stress,
ethanol
(EtOH)
may
aggravate
ischemia/reperfusion
(I/R)-induced
brain
damage.
However,
the
effect
of
prolonged
alcohol
intake
on
acute
injury
remains
ambiguous.
As
part
mitogen-activated
protein
kinase
(MAPK)
family,
p38γ
involved
in
ferroptosis
various
diseases.
This
study
explored
how
effects
chronic
EtOH
consumption
caused
cerebral
I/R.
Brain
damage
was
induced
mice
via
administration
liquid
alcohol-containing
diet
for
8
weeks,
middle
artery
occlusion
reperfusion
(MCAO/R),
or
combination
both.
We
verified
significantly
exacerbated
MCAO/R-induced
damage,
inflammation.
Notably,
levels
were
increased
experimental
mouse
cell
models.
knockdown
markedly
attenuated
tissue
inflammatory
infiltration
+
MCAO/R-treated
mice.
Mechanistic
experiments
revealed
regulate
through
p53/SLC7A11
pathway.
Overall,
our
results
indicate
crucial
regulating
EtOH-
I/R-induced
modulating
Otolaryngology,
Journal Year:
2025,
Volume and Issue:
unknown
Published: April 7, 2025
Abstract
Objective
Although
previous
studies
suggest
an
increased
stroke
risk
in
head
and
neck
cancer
(HNC)
survivors,
the
with
various
treatment
modalities,
including
radiotherapy,
is
less
certain.
This
study
investigates
incidence
HNC
patients,
how
different
treatments
influence
risk.
Data
Sources
A
literature
search
of
PubMed,
Scopus,
Embase
was
conducted.
Review
Methods
We
included
all
primary
assessing
as
outcome
patients
aged
18
older,
regardless
subtype
or
modality.
Incidence
rates
were
pooled
by
reconstructing
individual
patient
time‐to‐event
data
from
survival
curves.
Random‐effects
meta‐analyses
employed
to
compare
between
healthy
controls,
groups.
Results
In
total,
15
(N
=
2,295,447
patients)
analyses.
Among
surviving
occurred
at
a
rate
1%
per
year
(10%
10
years
15%
cumulatively).
Meta‐analyses
showed
that
had
significantly
higher
compared
controls
(hazard
ratio
[HR]
1.45;
95%
CI:
1.27‐1.65;
I
2
:
20%).
radiotherapy
alone
surgery
(HR
1.66;
1.35‐2.03;
0%).
Patients
who
received
any
form
those
without
1.47;
1.29‐1.68;
60%).
definitive
chemoradiotherapy
heightened
1.28;
1.09‐1.49;
86%).
Conclusion
face
elevated
risk,
especially
treated
radiotherapy.
underscores
need
for
surveillance
tailored
preventive
strategies
reduce
this
vulnerable
population.
Cell Death Discovery,
Journal Year:
2024,
Volume and Issue:
10(1)
Published: July 5, 2024
Ionizing
radiation
has
been
pivotal
in
cancer
therapy
since
its
discovery.
Despite
therapeutic
benefits,
IR
causes
significant
acute
and
chronic
complications
due
to
DNA
damage
the
generation
of
reactive
oxygen
species,
which
harm
nucleic
acids,
lipids,
proteins.
While
cells
are
more
vulnerable
ionizing
their
inefficiency
repairing
damage,
healthy
irradiated
area
also
suffer.
Various
types
cell
death
occur,
including
apoptosis,
necrosis,
pyroptosis,
autophagy-dependent
death,
immunogenic
ferroptosis.
Ferroptosis,
driven
by
iron-dependent
lipid
peroxide
accumulation,
recognized
as
crucial
therapy's
effects
complications,
with
extensive
research
across
various
tissues.
This
review
aims
summarize
pathways
involved
radiation-related
ferroptosis,
findings
different
organs,
drugs
targeting
ferroptosis
mitigate
harmful
effects.
Mini-Reviews in Medicinal Chemistry,
Journal Year:
2024,
Volume and Issue:
24(13), P. 1262 - 1276
Published: Jan. 29, 2024
Since
ferroptosis
was
reported
in
2012,
its
application
prospects
various
diseases
have
been
widely
considered,
initially
as
a
treatment
direction
for
tumors.
Recent
studies
shown
that
is
closely
related
to
the
occurrence
and
development
of
atherosclerosis.
The
primary
mechanism
affect
atherosclerosis
through
intracellular
iron
homeostasis,
ROS
lipid
peroxide
production
metabolism,
variety
signaling
pathways.
Inhibition
effective
inhibiting
atherosclerosis,
it
can
bring
new
treating
In
this
review,
we
discuss
focus
on
relationship
between
summarize
different
types
inhibitors
studied,
some
issues
worthy
attention
by
targeting
ferroptosis.
The Science of The Total Environment,
Journal Year:
2024,
Volume and Issue:
947, P. 174540 - 174540
Published: July 6, 2024
The
cardiovascular
system
effects
of
environmental
low-dose
radiation
exposure
on
practitioners
remain
uncertain
and
require
further
investigation.
aim
this
study
was
to
initially
investigate
explore
the
mechanisms
by
which
may
contribute
atherosclerosis
through
a
multi-omics
joint
comprehensive
basic
experiment.
Biomolecules,
Journal Year:
2024,
Volume and Issue:
14(7), P. 879 - 879
Published: July 22, 2024
This
study
sought
to
explore
potential
roles
of
endothelial
ferroptosis
in
radiation-associated
atherosclerosis
(RAA)
and
molecular
mechanisms
behind
this
phenomenon.
Here,
an
vivo
RAA
mouse
model
was
used
treated
with
inhibitors.
We
found
that
the
group
had
a
higher
plaque
burden
reduction
cells
increased
lipid
peroxidation
compared
control
group,
while
ameliorated
by
liproxstatin-1.
In
vitro
experiments
further
confirmed
radiation
induced
occurrence
human
artery
(HAECs).
Then,
proteomics
analysis
HAECs
identified
domain-containing
protein
2
(DDHD2)
as
co-differentially
expressed
protein,
which
enriched
metabolism
pathway.
addition,
level
elevated
DDHD2-knockdown
HAECs.
Mechanistically,
significant
decrease
mRNA
expression
glutathione
peroxidase
4
(GPX4)
observed
following
DDHD2
knockdown.
Co-immunoprecipitation
assays
indicated
interaction
between
nuclear
factor
erythroid
2-related
(Nrf2).
The
downregulation
Nrf2
also
detected
conclusion,
our
findings
suggest
radiation-induced
accelerates
atherosclerosis,
is
regulatory
through
Nrf2/GPX4