Drug Development Research,
Год журнала:
2024,
Номер
85(8)
Опубликована: Дек. 1, 2024
ABSTRACT
Cerebral
ischemia/reperfusion
injury
is
one
of
the
main
causes
neuronal
damage.
Neuron
ferroptosis
and
microglia
polarization
are
considered
as
critical
processes
during
cerebral
ischemia/reperfusion.
Adipocyte
enhancer‐binding
protein
1
(AEBP1)
usually
acts
a
transcriptional
repressor
which
involved
in
various
diseases.
However,
it
still
remains
unknown
whether
AEBP1
could
have
important
roles
regulating
neuron
injury.
The
oxygen‐glucose
deprivation
reperfusion
(OGD/R)‐treated
cells
middle
artery
occlusion
(MCAO)‐treated
mice
were
used
vitro
vivo
models.
differentially
expressed
factors
analyzed
according
to
GEO
datasets.
Relative
mRNA
expression
levels
detected
by
qRT‐PCR
western
blot
analysis.
Cell
viability
was
measured
CCK‐8
assay.
ROS,
GSH
iron
contents
using
specifical
assay
kits.
CD26
CD206
immunofluorescence
Inflammatory
cytokines
ELISA.
association
between
PRKCA
assessed
luciferase
reporter
ChIP
analyses.
damage
TTC
staining
neurological
deficit
score.
Transcription
factor
increased
OGD/R‐treated
HT22
BV2
cells.
silencing
attenuated
OGD/R‐induced
cell
through
increasing
viability,
GPX4
levels,
decreasing
ACSL4
levels.
knockdown
promoted
M2
CD206‐positive
Arg‐1
level,
reducing
iNOS,
TNF‐α,
IL‐1β
IL‐6
transcriptionally
repressed
expression,
further
regulated
PI3K/Akt
signaling
activation.
Inhibition
or
reversed
effects
on
polarization.
downregulation
infarct
size
scores
MCAO‐treated
mice.
mitigated
activating
signaling,
indicating
potentially
protective
action
Frontiers in Pharmacology,
Год журнала:
2024,
Номер
15
Опубликована: Май 23, 2024
Ferroptosis
is
a
non-apoptotic
mode
of
programmed
cell
death
characterized
by
iron
dependence
and
lipid
peroxidation.
Since
the
ferroptosis
was
proposed,
researchers
have
revealed
mechanisms
its
formation
continue
to
explore
effective
inhibitors
in
disease.
Recent
studies
shown
correlation
between
pathological
neurodegenerative
diseases,
as
well
diseases
involving
tissue
or
organ
damage.
Acting
on
ferroptosis-related
targets
may
provide
new
strategies
for
treatment
ferroptosis-mediated
diseases.
This
article
specifically
describes
metabolic
pathways
summarizes
reported
action
natural
synthetic
small
molecule
their
efficacy
The
paper
also
treatments
such
gene
therapy,
nanotechnology,
summarises
challenges
encountered
clinical
translation
inhibitors.
Finally,
relationship
other
modes
discussed,
hopefully
paving
way
future
drug
design
discovery.
Pharmaceuticals,
Год журнала:
2025,
Номер
18(3), С. 325 - 325
Опубликована: Фев. 26, 2025
The
emergence
of
nanotechnology
in
medicine,
particularly
using
iron
oxide
nanoparticles
(IONPs),
may
impact
cancer
treatment
strategies.
IONPs
exhibit
unique
properties,
such
as
superparamagnetism,
biocompatibility,
and
ease
surface
modification,
making
them
ideal
candidates
for
imaging,
therapeutic
interventions.
Their
application
targeted
drug
delivery,
especially
with
traditional
chemotherapeutic
agents
like
cisplatin,
has
shown
potential
overcoming
limitations
low
bioavailability
systemic
toxicity
chemotherapies.
Moreover,
IONPs,
by
releasing
ions,
can
induce
ferroptosis,
a
form
iron-dependent
cell
death,
which
offers
promising
pathway
to
reverse
radio-
chemoresistance
therapy.
In
particular,
demonstrate
significant
radiosensitisers,
enhancing
the
effects
radiotherapy
promoting
reactive
oxygen
species
(ROS)
generation,
lipid
peroxidation,
modulating
tumour
microenvironment
stimulate
antitumour
immune
responses.
This
review
explores
multifunctional
roles
radiosensitisation
through
ferroptosis
induction,
highlighting
their
promise
advancing
head
neck
cancers.
Additional
research
is
crucial
fully
addressing
clinical
settings,
offering
novel
approach
personalised
treatment.
Annals of Medicine,
Год журнала:
2025,
Номер
57(1)
Опубликована: Март 4, 2025
It
is
now
understood
that
iron
crosses
the
blood-brain
barrier
via
a
complex
metabolic
regulatory
network
and
participates
in
diverse
critical
biological
processes
within
central
nervous
system,
including
oxygen
transport,
energy
metabolism,
synthesis
catabolism
of
myelin
neurotransmitters.
During
brain
development,
distributed
throughout
brain,
playing
pivotal
role
key
such
as
neuronal
myelination,
neurotransmitter
synthesis.
In
physiological
aging,
can
selectively
accumulate
specific
regions,
impacting
cognitive
function
leading
to
intracellular
redox
imbalance,
mitochondrial
dysfunction,
lipid
peroxidation,
thereby
accelerating
aging
associated
pathologies.
Furthermore,
accumulation
may
be
primary
contributor
neurodegenerative
diseases
Alzheimer's
Parkinson's
diseases.
Comprehending
diseases,
utilizing
iron-sensitive
Magnetic
Resonance
Imaging
(MRI)
technology
for
timely
detection
or
prediction
abnormal
neurological
states,
implementing
appropriate
interventions
instrumental
preserving
normal
system
function.
Frontiers in Cellular Neuroscience,
Год журнала:
2024,
Номер
18
Опубликована: Окт. 15, 2024
Ferroptosis
represents
an
iron
−
and
lipid
peroxidation
(LPO)-mediated
form
of
regulated
cell
death
(RCD).
Recent
evidence
strongly
suggests
the
involvement
ferroptosis
in
various
neurodegenerative
diseases
(NDs),
particularly
Alzheimer’s
disease
(AD),
Parkinson’s
(PD),
Huntington’s
(HD),
multiple
sclerosis
(MS),
amyotrophic
lateral
(ALS),
among
others.
The
treatment
poses
both
opportunities
challenges
context
ND.
This
review
provides
a
comprehensive
overview
characteristic
features,
induction
inhibition
ferroptosis,
highlighting
inhibitor
underlying
mechanisms
responsible
for
its
occurrence.
Moreover,
explores
how
these
contribute
to
pathogenesis
progression
major
disorders.
Additionally,
it
presents
novel
insights
into
role
ND
summarizes
recent
advancements
development
therapeutic
approaches
targeting
ferroptosis.
These
hold
potential
guide
future
strategies
aimed
at
effectively
managing
debilitating
medical
conditions.
Biomolecules,
Год журнала:
2024,
Номер
14(11), С. 1443 - 1443
Опубликована: Ноя. 13, 2024
Ferroptosis,
an
iron-dependent
form
of
regulated
cell
death
driven
by
lipid
peroxidation,
has
emerged
as
a
critical
pathway
in
cancer
biology.
This
review
delves
into
the
epigenetic
mechanisms
that
modulate
ferroptosis
cells,
focusing
on
how
DNA
methylation,
histone
modifications,
and
non-coding
RNAs
influence
expression
function
essential
genes
involved
this
process.
By
unraveling
complex
interplay
between
these
ferroptosis,
article
sheds
light
novel
gene
targets
functional
insights
could
pave
way
for
innovative
treatments
to
enhance
therapeutic
efficacy
overcome
resistance
therapy.
Cancers,
Год журнала:
2025,
Номер
17(5), С. 800 - 800
Опубликована: Фев. 26, 2025
NINJ1
was
initially
recognized
for
its
role
in
nerve
regeneration
and
cellular
adhesion.
Subsequent
studies
have
uncovered
participation
cancer
progression,
where
regulates
critical
steps
tumor
metastasis,
such
as
cell
migration
invasion.
More
recently,
has
emerged
a
multifunctional
protein
mediating
plasma
membrane
rupture
(PMR)
several
lytic
death
processes,
including
apoptosis,
necroptosis,
pyroptosis.
However,
ferroptosis-an
iron-dependent
form
of
characterized
by
lipid
peroxidation-remained
unclear
until
2024.
Ferroptosis
is
suppression
mechanism
that
may
be
particularly
relevant
to
detached
metastatic
cells.
This
review
explores
the
invasion
focusing
on
regulation
ferroptosis
via
non-canonical
distinct
from
other
deaths.
We
discuss
process
implications
metastasis.
Furthermore,
we
recent
highlighting
diverse
roles
regulation,
canonical
function
PMR
modulating
intracellular
levels
glutathione
(GSH)
coenzyme
A
(CoA)
interaction
with
xCT
anti-porter.
Given
been
associated
suppression,
elimination
treatment-resistant
cells,
dormancy,
NINJ1's
modulation
presents
promising
therapeutic
target
inhibiting
Understanding
dual
promoting
or
restraining
depending
context
could
open
avenues
novel
anti-cancer
strategies
enhance
ferroptotic
vulnerability
tumors.
Frontiers in Immunology,
Год журнала:
2025,
Номер
16
Опубликована: Март 11, 2025
Ferroptosis,
an
iron-dependent
form
of
regulated
cell
death
driven
by
lipid
peroxidation,
plays
a
pivotal
role
in
various
physiological
and
pathological
processes.
In
this
review,
we
summarize
the
core
mechanisms
ferroptosis,
emphasizing
its
intricate
connections
to
metabolism,
including
fatty
acid
synthesis,
phospholipid
remodeling,
oxidation
dynamics.
We
further
highlight
advancements
detection
technologies,
such
as
fluorescence
imaging,
lipidomics,
vivo
PET
which
have
deepened
our
understanding
ferroptotic
regulation.
Additionally,
discuss
ferroptosis
human
diseases,
where
it
acts
double-edged
sword,
contributing
cancer
while
also
driving
ischemia-reperfusion
injury
neurodegeneration.
Finally,
explore
therapeutic
strategies
aimed
at
either
inducing
or
inhibiting
iron
chelation,
antioxidant
modulation,
lipid-targeted
interventions.
By
integrating
mechanistic
insights,
disease
relevance,
potential,
review
provides
comprehensive
perspective
on
crucial
interface
between
metabolism
oxidative
stress.