Discover Nano,
Journal Year:
2025,
Volume and Issue:
20(1)
Published: April 24, 2025
Cancer
treatments
often
exploit
oxidative
stress
to
selectively
kill
tumour
cells
by
disrupting
their
lipid
peroxidation
membranes
and
inhibiting
antioxidant
enzymes.
However,
plays
a
dual
role
in
cancer
progression,
acting
as
both
promoter
suppressor.
Balancing
through
therapy
remains
challenge,
excessive
activity
may
compromise
the
efficacy
of
chemotherapy
radiotherapy.
This
review
explores
antioxidants
mitigating
while
maintaining
treatment
efficacy.
It
highlights
recent
advancements
nanotechnology-based
targeted
delivery
optimize
therapeutic
outcomes.
A
comprehensive
literature
was
conducted
using
reputable
databases,
including
PubMed,
Scopus,
Web
Science,
ScienceDirect.
The
search
focused
on
publications
from
past
five
years
(2020-2025),
supplemented
relevant
studies
earlier
years.
Keywords
such
"antioxidants,"
"lipid
peroxidation,"
"nanotechnology
therapy,"
"oxidative
stress"
were
utilized.
Relevant
articles
critically
analysed,
graphical
illustrations
created.
Emerging
evidence
suggests
that
nanoparticles,
liposomes,
polymeric
metal-organic
frameworks,
others,
can
effectively
encapsulate
control
release
minimizing
systemic
toxicity.
Stimuli-responsive
carriers
with
tumour-specific
targeting
mechanisms
further
enhance
delivery.
Studies
indicate
these
strategies
help
preserve
normal
cells,
mitigate
stress-related
damage,
improve
challenges
bioavailability,
stability,
potential
interactions
standard
therapies
remain.
Integrating
nanotechnology
antioxidant-based
interventions
presents
promising
approach
for
optimizing
therapy.
Future
research
should
focus
refining
modulation
strategies,
assessing
profiles
during
treatment,
employing
biomarkers
determine
optimal
dosing.
balanced
use
adverse
effects.
Signal Transduction and Targeted Therapy,
Journal Year:
2024,
Volume and Issue:
9(1)
Published: Oct. 14, 2024
Iron,
an
essential
mineral
in
the
body,
is
involved
numerous
physiological
processes,
making
maintenance
of
iron
homeostasis
crucial
for
overall
health.
Both
overload
and
deficiency
can
cause
various
disorders
human
diseases.
Ferroptosis,
a
form
cell
death
dependent
on
iron,
characterized
by
extensive
peroxidation
lipids.
Unlike
other
kinds
classical
unprogrammed
death,
ferroptosis
primarily
linked
to
disruptions
metabolism,
lipid
peroxidation,
antioxidant
system
imbalance.
Ferroptosis
regulated
through
transcription,
translation,
post-translational
modifications,
which
affect
cellular
sensitivity
ferroptosis.
Over
past
decade
or
so,
diseases
have
been
as
part
their
etiology,
including
cancers,
metabolic
disorders,
autoimmune
diseases,
central
nervous
cardiovascular
musculoskeletal
Ferroptosis-related
proteins
become
attractive
targets
many
major
that
are
currently
incurable,
some
regulators
shown
therapeutic
effects
clinical
trials
although
further
validation
potential
needed.
Therefore,
in-depth
analysis
its
molecular
mechanisms
may
offer
additional
strategies
prevention
treatment.
In
this
review,
we
discuss
significance
contribution
etiology
development
along
with
evidence
supporting
targeting
approach.
Importantly,
evaluate
recent
promising
interventions,
providing
guidance
future
targeted
treatment
therapies
against
MedComm,
Journal Year:
2023,
Volume and Issue:
4(4)
Published: June 26, 2023
Brain
iron
homeostasis
is
maintained
through
the
normal
function
of
blood-brain
barrier
and
regulation
at
systemic
cellular
levels,
which
fundamental
to
brain
function.
Excess
can
catalyze
generation
free
radicals
Fenton
reactions
due
its
dual
redox
state,
thus
causing
oxidative
stress.
Numerous
evidence
has
indicated
diseases,
especially
stroke
neurodegenerative
are
closely
related
mechanism
imbalance
in
brain.
For
one
thing,
diseases
promote
accumulation.
another,
accumulation
amplifies
damage
nervous
system
exacerbates
patients'
outcomes.
In
addition,
triggers
ferroptosis,
a
newly
discovered
iron-dependent
type
programmed
cell
death,
neurodegeneration
received
wide
attention
recent
years.
this
context,
we
outline
metabolism
focus
on
current
stroke,
Alzheimer's
disease,
Parkinson's
disease.
Meanwhile,
also
discuss
ferroptosis
simultaneously
enumerate
drugs
for
chelators
inhibitors.
Journal of Pineal Research,
Journal Year:
2024,
Volume and Issue:
76(2)
Published: March 1, 2024
Abstract
Parkinson's
disease
(PD)
is
a
neurodegenerative
disorder
characterized
by
the
loss
of
dopaminergic
(DA)
neurons
and
aggregation
α‐synuclein
(α‐syn).
Ferroptosis,
form
cell
death
induced
iron
accumulation
lipid
peroxidation,
involved
in
pathogenesis
PD.
It
unknown
whether
melatonin
receptor
1
(MT1)
modulates
α‐syn
ferroptosis
Here,
we
used
preformed
fibrils
(PFFs)
to
induce
PD
models
vivo
vitro.
In
mice,
led
increased
deposition
ferroptosis.
MT1
knockout
exacerbated
these
changes
resulted
more
DA
neuronal
severe
motor
impairment.
also
suppressed
Sirt1/Nrf2/Ho1/Gpx4
pathway,
reducing
resistance
ferroptosis,
inhibited
expression
ferritin
Fth1,
leading
release
ferrous
ions.
vitro
experiments
confirmed
findings.
Knockdown
enhanced
PFF‐induced
intracellular
pathway
Fth1
protein,
thereby
aggravating
Conversely,
overexpression
reversed
effects.
Our
findings
reveal
novel
mechanism
which
activation
prevents
α‐syn‐induced
PD,
highlighting
neuroprotective
role
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(3), P. 298 - 298
Published: Feb. 28, 2024
Ferroptosis
is
a
type
of
programmed
cell
death
that
differs
from
apoptosis,
autophagy,
and
necrosis
related
to
several
physio-pathological
processes,
including
tumorigenesis,
neurodegeneration,
senescence,
blood
diseases,
kidney
disorders,
ischemia–reperfusion
injuries.
linked
iron
accumulation,
eliciting
dysfunction
antioxidant
systems,
which
favor
the
production
lipid
peroxides,
membrane
damage,
ultimately,
death.
Thus,
signaling
pathways
evoking
ferroptosis
are
strongly
associated
with
those
protecting
cells
against
excess
and/or
lipid-derived
ROS.
Here,
we
discuss
interaction
between
metabolic
particular
focus
on
transcription
factors
implicated
in
regulation
ferroptosis,
either
as
triggers
peroxidation
or
defense
pathways.
Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
14
Published: Jan. 8, 2024
The
incidence
rate
of
depression,
a
mental
disorder,
is
steadily
increasing
and
has
the
potential
to
become
major
global
disability
factor.
Given
complex
pathological
mechanisms
involved
in
use
conventional
antidepressants
may
lead
severe
complications
due
their
side
effects.
Hence,
there
critical
need
explore
development
novel
antidepressants.
Ferroptosis,
newly
recognized
form
cell
death,
been
found
be
closely
linked
onset
depression.
Several
studies
have
indicated
that
certain
active
ingredients
can
ameliorate
depression
by
modulating
ferroptosis
signaling
pathway.
Notably,
traditional
Chinese
medicine
(TCM)
TCM
prescriptions
demonstrated
promising
antidepressant
effects
previous
investigations
owing
unique
advantages
therapy.
Building
upon
these
findings,
our
objective
was
review
recent
relevant
research
provide
new
insights
directions
for
application
innovative
strategies.
Redox Biology,
Journal Year:
2024,
Volume and Issue:
75, P. 103268 - 103268
Published: July 17, 2024
Intracerebral
hemorrhage
(ICH)
is
a
prevalent
hemorrhagic
cerebrovascular
emergency.
Alleviating
neurological
damage
in
the
early
stages
of
ICH
critical
for
enhancing
patient
prognosis
and
survival
rate.
A
novel
form
cell
death
called
ferroptosis
intimately
linked
to
hemorrhage-induced
brain
tissue
injury.
Although
studies
have
demonstrated
significant
preventive
impact
bovine
serum
albumin-stabilized
selenium
nanoparticles
(BSA-SeNPs)
against
disorders
connected
system,
neuroprotective
effect
on
stroke
mechanism
remain
unknown.
Therefore,
based
favorable
biocompatibility
BSA-SeNPs,
h-ICH
(hippocampus-intracerebral
hemorrhage)
model
was
constructed
perform
BSA-SeNPs
therapy.
As
expected,
these
could
effectively
improve
cognitive
deficits
ameliorate
hippocampal
neuron.
Furthermore,
reverse
morphology
mitochondria
enhanced
mitochondrial
function,
evidenced
by
respiration
function
(OCR)
membrane
potential
(MMP).
Mechanistically,
efficiently
activate
Nrf2
enhance
expression
antioxidant
GPX4
at
mRNA
protein
levels,
further
inhibit
lipid
peroxidation
production
erastin-induced
ferroptotic
damages.
Taken
together,
this
study
not
only
sheds
light
clinical
application
but
also
provides
its
newly
theoretical
support
strategy
intervention
treatment
impairment
following
ICH.
MedComm,
Journal Year:
2024,
Volume and Issue:
5(12)
Published: Nov. 20, 2024
Ferroptosis
is
a
nonapoptotic
form
of
cell
death
characterized
by
iron-dependent
lipid
peroxidation
in
membrane
phospholipids.
Since
its
identification
2012,
extensive
research
has
unveiled
involvement
the
pathophysiology
numerous
diseases,
including
cancers,
neurodegenerative
disorders,
organ
injuries,
infectious
autoimmune
conditions,
metabolic
and
skin
diseases.
Oxidizable
lipids,
overload
iron,
compromised
antioxidant
systems
are
known
as
critical
prerequisites
for
driving
overwhelming
peroxidation,
ultimately
leading
to
plasma
rupture
ferroptotic
death.
However,
precise
regulatory
networks
governing
ferroptosis
ferroptosis-targeted
therapy
these
diseases
remain
largely
undefined,
hindering
development
pharmacological
agonists
antagonists.
In
this
review,
we
first
elucidate
core
mechanisms
summarize
epigenetic
modifications
(e.g.,
histone
modifications,
DNA
methylation,
noncoding
RNAs,
N6-methyladenosine
modification)
nonepigenetic
genetic
mutations,
transcriptional
regulation,
posttranslational
modifications).
We
then
discuss
association
between
disease
pathogenesis
explore
therapeutic
approaches
targeting
ferroptosis.
also
introduce
potential
clinical
monitoring
strategies
Finally,
put
forward
several
unresolved
issues
which
progress
needed
better
understand
hope
review
will
offer
promise
application
therapies
context
human
health
disease.