Briefings in Bioinformatics,
Journal Year:
2024,
Volume and Issue:
25(3)
Published: March 27, 2024
Ferroptosis
is
a
non-apoptotic,
iron-dependent
regulatory
form
of
cell
death
characterized
by
the
accumulation
intracellular
reactive
oxygen
species.
In
recent
years,
large
and
growing
body
literature
has
investigated
ferroptosis.
Since
ferroptosis
associated
with
various
physiological
activities
regulated
variety
cellular
metabolism
mitochondrial
activity,
been
closely
related
to
occurrence
development
many
diseases,
including
cancer,
aging,
neurodegenerative
ischemia-reperfusion
injury
other
pathological
death.
The
regulation
mainly
focuses
on
three
pathways:
system
Xc-/GPX4
axis,
lipid
peroxidation
iron
metabolism.
genes
involved
in
these
processes
were
divided
into
driver,
suppressor
marker.
Importantly,
small
molecules
or
drugs
that
mediate
expression
are
often
good
treatments
clinic.
Herein,
newly
developed
database,
named
'FERREG',
documented
(i)
providing
data
ferroptosis-related
diseases
occurrence,
progression
drug
response;
(ii)
explicitly
describing
molecular
mechanisms
underlying
each
regulation;
(iii)
fully
referencing
collected
cross-linking
them
available
databases.
Collectively,
FERREG
contains
51
targets,
718
regulators,
445
158
disease
responses.
can
be
accessed
at
https://idrblab.org/ferreg/.
Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
15
Published: May 23, 2024
Lung
cancer
is
the
leading
cause
of
global
cancer-related
deaths.
Platinum-based
chemotherapy
first-line
treatment
for
most
common
type
lung
cancer,
i.e.,
non-small-cell
(NSCLC),
but
its
therapeutic
efficiency
limited
by
chemotherapeutic
resistance.
Therefore,
it
vital
to
develop
effective
modalities
that
bypass
molecular
mechanisms
associated
with
Ferroptosis
a
form
non-apoptotic
regulated
cell
death
characterized
iron-dependent
lipid
peroxidation
(LPO).
crucial
proper
efficacy
cancer-associated
chemotherapies.
If
targeted
as
novel
mechanism,
ferroptosis
modulators
present
new
opportunities
increasing
chemotherapy.
Emerging
studies
have
revealed
pharmacological
induction
using
natural
compounds
boosts
in
or
drug-resistant
cancer.
In
this
review,
we
first
discuss
resistance
(or
chemoresistance)
and
introduce
core
behind
ferroptosis.
Then,
comprehensively
summarize
small-molecule
sourced
from
traditional
medicines
may
boost
anti-tumor
activity
current
agents
overcome
NSCLC.
Cumulatively,
suggest
ferroptosis-related
anticancer
could
serve
starting
point
NSCLC
inducing
ferroptosis,
highlighting
potential
regimens
used
chemoresistance
Phytomedicine,
Journal Year:
2024,
Volume and Issue:
132, P. 155876 - 155876
Published: July 14, 2024
Ferroptosis,
an
emerging
nonapoptotic,
modulated
cell
death
process
characterized
by
iron
accumulation
and
subsequent
lipid
peroxidation,
has
been
intimately
implicated
in
the
development
progression
of
ovarian
cancer
(OC).
Daphnetin
(Daph),
a
natural
product
isolated
from
Daphne
Korean
Nakai,
exhibits
anticancer
efficacy
against
various
solid
tumors.
However,
specific
role
potential
mechanism
underlying
Daph-mediated
modulation
ferroptosis
OC
cells
remain
elusive.
Theranostics,
Journal Year:
2024,
Volume and Issue:
14(15), P. 5826 - 5852
Published: Jan. 1, 2024
Ferroptosis,
an
iron-dependent
form
of
regulated
cell
death,
is
emerging
as
a
crucial
regulator
human
physiology
and
pathology.
Increasing
evidence
showcases
reciprocal
relationship
between
ferroptosis
dysregulated
metabolism,
propagating
pathogenic
vicious
cycle
that
exacerbates
pathology
diseases,
particularly
metabolic
disorders.
Consequently,
there
rapidly
growing
interest
in
developing
ferroptosis-based
therapeutics.
Therefore,
comprehensive
understanding
the
intricate
interplay
metabolism
could
provide
invaluable
resource
for
mechanistic
insight
therapeutic
development.
In
this
review,
we
summarize
important
substances
associated
pathways
initiation
progression,
outline
cascade
responses
disease
development,
overview
roles
mechanisms
introduce
methods
detection,
discuss
perspectives
ferroptosis,
which
collectively
aim
to
illustrate
view
basic,
translational,
clinical
science.
ACS Nano,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 3, 2025
Ferroptosis
is
a
classic
type
of
programmed
cell
death
characterized
by
iron
dependence,
which
closely
associated
with
many
diseases
such
as
cancer,
intestinal
ischemic
diseases,
and
nervous
system
diseases.
Transferrin
(Tf)
responsible
for
ferric-ion
delivery
owing
to
its
natural
Fe3+
binding
ability
plays
crucial
role
in
ferroptosis.
However,
Tf
not
considered
druggable
target
ferroptosis-associated
since
systemic
perturbation
would
dramatically
disrupt
blood
homeostasis.
Here,
we
reported
nonpharmaceutical,
noninvasive,
Tf-targeted
electromagnetic
intervention
technique
capable
desensitizing
ferroptosis
directivity.
First,
revealed
that
the
THz
radiation
had
significantly
decrease
affinity
between
via
molecular
dynamics
simulations,
modulation
was
strongly
wavelength-dependent.
This
result
provides
theoretical
feasibility
modulation-based
intervention.
Subsequent
extracellular
cellular
chromogenic
activity
assays
indicated
field
at
8.7
μm
(i.e.,
34.5
THz)
inhibited
most
bound
Tf,
wavelength
good
agreement
simulated
one.
Then,
functional
demonstrated
levels
intracellular
Fe2+,
lipid
peroxidation,
malondialdehyde
(MDA)
were
all
reduced
cells
treated
this
wave.
Furthermore,
deposition,
MDA
disease
model
induced
ischemia-reperfusion
injury
could
be
nearly
eliminated
same
radiation,
validating
wave-induced
desensitization
vivo.
Together,
work
preclinical
exemplar
irradiation-stimulated
predicts
an
innovative,
wave-based
therapeutic
method
future.
Cancer Drug Resistance,
Journal Year:
2025,
Volume and Issue:
8(1)
Published: Jan. 6, 2025
Ferroptosis
is
an
iron-dependent
form
of
programmed
cell
death
induced
by
lipid
peroxidation.
This
process
regulated
signaling
pathways
associated
with
redox
balance,
iron
metabolism,
and
metabolism.
Cancer
cells'
increased
demand
makes
them
especially
susceptible
to
ferroptosis,
significantly
influencing
cancer
development,
therapeutic
response,
metastasis.
Recent
findings
indicate
that
cells
can
evade
ferroptosis
downregulating
key
related
this
process,
contributing
drug
resistance.
underscores
the
possibility
modulating
as
approach
counteract
resistance
enhance
efficacy.
review
outlines
involved
in
their
interactions
cancer-related
pathways.
We
also
highlight
current
understanding
resistance,
offering
insights
into
how
targeting
provide
novel
approaches
for
drug-resistant
cancers.
Finally,
we
explore
potential
ferroptosis-inducing
compounds
examine
challenges
opportunities
development
evolving
field.
Translational Gastroenterology and Hepatology,
Journal Year:
2025,
Volume and Issue:
10, P. 7 - 7
Published: Jan. 1, 2025
Gastrointestinal
adenocarcinomas
(GIACs)
are
common
malignant
tumors
with
poor
prognosis
in
the
world.
Ferroptosis,
characterized
by
accumulation
of
intracellular
iron
and
lipid
reactive
oxygen
species,
emerges
as
a
pivotal
process
tumorigenesis
cancer
advancement.
However,
implications
ferroptosis-related
genes
GIAC
remain
to
be
elucidated.
This
study
aimed
at
exploring
potential
role
on
treatment
GIAC.
In
our
study,
comprehensive
clinical,
transcriptomic,
and/or
genomic
data
were
acquired
from
The
Cancer
Genome
Atlas
(TCGA),
Cell
Line
Encyclopedia
(CCLE),
Genomics
Drug
Sensitivity
(GDSC),
Gene
Expression
Omnibus
(GEO).
We
formulated
ferroptosis-score
within
TCGA
cohort
through
gene
set
variation
analysis
(GSVA)
subsequently
validated
4
GEO
datasets
(GSE84437,
GSE17536,
GSE103479,
GSE19417).
sensitivity
immunotherapy
efficacy
analyzed
GDSC
dataset
PRJEB25780
cohort,
respectively.
was
significantly
associated
favorable
overall
survival
both
training
[TCGA:
P=0.003;
hazard
ratio
(HR),
0.67,
95%
confidence
interval
(95%
CI):
0.52-0.87]
across
four
validation
cohorts
(GSE17536:
P=0.03;
HR,
0.57,
CI:
0.34-0.96;
GSE19417:
P=0.047;
0.53,
0.28-1.01;
GSE84437:
P=0.004;
0.68,
0.51-0.90;
GSE103479:
0.55,
0.32-0.96).
Furthermore,
correlated
activation
DNA
damage
repair
pathway
resistance
cisplatin.
Notably,
GIACs
low
ferroptosis-scores
exhibited
heightened
expression
immune
checkpoint
molecules
such
programmed
death-(ligand)
1
cytotoxic
T
lymphocyte
antigen-4,
elevated
densities
tumor-infiltrating
CD8+
cells,
response
pembrolizumab
monotherapy.
Our
findings
delineated
clinical
relevance
demonstrated
utility
predicting
effectiveness.
Frontiers in Immunology,
Journal Year:
2025,
Volume and Issue:
16
Published: Feb. 11, 2025
Ferroptosis,
an
iron-dependent
form
of
regulated
cell
death,
is
characterized
by
the
lethal
accumulation
lipid
peroxides
on
cellular
membranes.
It
not
only
inhibits
tumor
growth
but
also
enhances
immunotherapy
responses
and
overcomes
drug
resistance
in
cancer
therapy.
The
inhibition
cystine-glutamate
antiporter,
system
Xc-,
induces
ferroptosis.
Imidazole
ketone
erastin
(IKE),
inhibitor
Xc-
functional
subunit
solute
carrier
family
7
member
11
(SLC7A11),
effective
metabolically
stable
inducer
ferroptosis
with
potential
vivo
applications.
However,
cells
exhibited
differential
sensitivity
to
IKE-induced
intrinsic
factors
determining
remain
be
explored
improve
its
efficacy.
Bulk
RNA-sequencing
data
from
hepatocellular
carcinoma
(HCC)
normal
liver
tissues
were
collected
Cancer
Genome
Atlas
(TCGA)
Genotype-Tissue
Expression
(GTEx)
databases.
Differentially
expressed
genes
identified
intersected
ferroptosis-related
(FRGs)
listed
FerrDb
database,
yielding
identification
13
distinct
FRGs.
A
signature
index
model
(Risk
Score)
was
developed
predict
HCC
prognosis.
And
SLC7A11
NAD(P)H
quinone
dehydrogenase
1
(NQO1)
as
candidate
FRGs
indicating
poor
prognosis
HCC.
Dicoumarol
(DIC),
NQO1,
subsequently
employed
assess
sensitizing
effects
IKE
treatment.
In
lines
subcutaneous
xenograft
model,
combined
suppression
NQO1
significantly
enhanced
inhibitory
effect
inducing
conclusion,
our
findings
demonstrate
that
DIC
sensitized
Moreover,
drugs
enhance
susceptibility
could
provide
novel
therapeutic
strategies
for
treatment
Antioxidants,
Journal Year:
2025,
Volume and Issue:
14(2), P. 231 - 231
Published: Feb. 18, 2025
With
the
continued
exploration
of
universe,
there
is
an
increasingly
urgent
need
to
address
health
challenges
arising
from
spaceflight.
In
space,
astronauts
are
exposed
radiation,
confinement
and
isolation,
circadian
rhythm
dysregulation,
microgravity
conditions
that
different
those
on
Earth.
These
risk
factors
jeopardize
astronauts'
health,
thus
affecting
quality
space
missions.
Among
these
factors,
gravitational
changes
influence
balance
between
oxidation
antioxidants,
stimulating
production
reactive
oxygen
species
(ROS),
finally
leading
oxidative
stress
(OS).
OS
leads
damage
biomolecules
such
as
lipids,
proteins,
DNA,
which
causes
development
various
diseases.
The
occurrence
increased
in
affects
multiple
systems,
including
musculoskeletal,
cardiovascular,
nervous,
immune
systems.
this
review,
we
discuss
mechanisms
OS,
physiological
effects
systems
caused
by
environment,
potential
treatments
for
OS.
Finally,
treatment
strategies
summarized,
providing
some
promising
approaches
protecting
future
exploration.