Cell Death and Differentiation,
Journal Year:
2022,
Volume and Issue:
29(3), P. 467 - 480
Published: Jan. 24, 2022
Ferroptosis
is
an
iron-dependent
form
of
non-apoptotic
cell
death
characterized
by
excessive
lipid
peroxidation
and
associated
with
a
plethora
pathological
conditions
in
the
liver.
Emerging
evidence
supports
notion
that
dysregulated
metabolic
pathways
impaired
iron
homeostasis
play
role
progression
liver
disease
via
ferroptosis.
Although
molecular
mechanisms
which
ferroptosis
causes
are
poorly
understood,
several
ferroptosis-associated
genes
have
been
implicated
disease.
Here,
we
review
physiological
processing
nutrients,
our
current
understanding
metabolism,
characteristics
ferroptosis,
regulate
In
addition,
summarize
pathogenesis
disease,
including
injury,
non-alcoholic
steatohepatitis,
fibrosis,
cirrhosis,
hepatocellular
carcinoma.
Finally,
discuss
therapeutic
potential
targeting
for
managing
Cancer Communications,
Journal Year:
2018,
Volume and Issue:
38(1), P. 1 - 14
Published: May 21, 2018
Abstract
Reprogramming
of
lipid
metabolism
is
a
newly
recognized
hallmark
malignancy.
Increased
uptake,
storage
and
lipogenesis
occur
in
variety
cancers
contribute
to
rapid
tumor
growth.
Lipids
constitute
the
basic
structure
membranes
also
function
as
signaling
molecules
energy
sources.
Sterol
regulatory
element‐binding
proteins
(SREBPs),
family
membrane‐bound
transcription
factors
endoplasmic
reticulum,
play
central
role
regulation
metabolism.
Recent
studies
have
revealed
that
SREBPs
are
highly
up‐regulated
various
promote
SREBP
cleavage‐activating
protein
key
transporter
trafficking
activation
well
critical
glucose
sensor,
thus
linking
de
novo
synthesis.
Targeting
altered
metabolic
pathways
has
become
promising
anti‐cancer
strategy.
This
review
summarizes
recent
progress
our
understanding
malignancy,
highlights
potential
molecular
targets
their
inhibitors
for
cancer
treatment.
PLoS Biology,
Journal Year:
2018,
Volume and Issue:
16(5), P. e2006203 - e2006203
Published: May 24, 2018
Ferroptosis
is
a
cell
death
process
driven
by
damage
to
membranes
and
linked
numerous
human
diseases.
caused
loss
of
activity
the
key
enzyme
that
tasked
with
repairing
oxidative
membranes-glutathione
peroxidase
4
(GPX4).
GPX4
normally
removes
dangerous
products
iron-dependent
lipid
peroxidation,
protecting
from
this
type
damage;
when
fails,
ferroptosis
ensues.
distinct
apoptosis,
necroptosis,
necrosis,
other
modes
death.
Several
mysteries
regarding
how
cells
die
during
remain
unsolved.
First,
drivers
peroxidation
are
not
yet
clear.
Second,
subcellular
location
lethal
peroxides
remains
an
outstanding
question.
Finally,
exactly
leads
unsolved
mystery.
Answers
these
questions
will
provide
insights
into
mechanisms
ferroptotic
associated
diseases,
as
well
new
therapeutic
strategies
for
such
Antioxidants,
Journal Year:
2019,
Volume and Issue:
9(1), P. 21 - 21
Published: Dec. 25, 2019
Cannabidiol
(CBD)
is
one
of
the
main
pharmacologically
active
phytocannabinoids
Cannabis
sativa
L.
CBD
non-psychoactive
but
exerts
a
number
beneficial
pharmacological
effects,
including
anti-inflammatory
and
antioxidant
properties.
The
chemistry
pharmacology
CBD,
as
well
various
molecular
targets,
cannabinoid
receptors
other
components
endocannabinoid
system
with
which
it
interacts,
have
been
extensively
studied.
In
addition,
preclinical
clinical
studies
contributed
to
our
understanding
therapeutic
potential
for
many
diseases,
diseases
associated
oxidative
stress.
Here,
we
review
biological
effects
its
synthetic
derivatives,
focusing
on
cellular,
antioxidant,
properties
CBD.
Angewandte Chemie International Edition,
Journal Year:
2021,
Volume and Issue:
60(23), P. 12971 - 12979
Published: March 27, 2021
Abstract
Photothermal
therapy
(PTT)
is
an
extremely
promising
tumor
therapeutic
modality.
However,
excessive
heat
inevitably
injures
normal
tissues
near
tumors,
and
the
damage
to
cancer
cells
caused
by
mild
hyperthermia
easily
repaired
stress‐induced
shock
proteins
(HSPs).
Thus,
maximizing
PTT
efficiency
minimizing
healthy
simultaneously
adopting
appropriate
temperatures
imperative.
Herein,
innovative
strategy
reported:
ferroptosis‐boosted
based
on
a
single‐atom
nanozyme
(SAzyme).
The
Pd
SAzyme
with
atom‐economical
utilization
of
catalytic
centers
exhibits
peroxidase
(POD)
glutathione
oxidase
(GSHOx)
mimicking
activities,
photothermal
conversion
performance,
which
can
result
in
ferroptosis
featuring
up‐regulation
lipid
peroxides
(LPO)
reactive
oxygen
species
(ROS).
accumulation
LPO
ROS
provides
powerful
approach
for
cleaving
HSPs,
enables
SAzyme‐mediated
mild‐temperature
PTT.
Annual Review of Cancer Biology,
Journal Year:
2018,
Volume and Issue:
3(1), P. 35 - 54
Published: Oct. 25, 2018
Ferroptosis
is
a
nonapoptotic,
iron-dependent
form
of
cell
death
that
can
be
activated
in
cancer
cells
by
natural
stimuli
and
synthetic
agents.
Three
essential
hallmarks
define
ferroptosis,
namely:
the
loss
lipid
peroxide
repair
capacity
phospholipid
hydroperoxidase
GPX4,
availability
redox-active
iron,
oxidation
polyunsaturated
fatty
acid
(PUFA)-containing
phospholipids.
Several
processes
including
RAS/MAPK
signaling,
amino
iron
metabolism,
ferritinophagy,
epithelial-to-mesenchymal
transition,
adhesion,
mevalonate
biosynthesis
modulate
susceptibility
to
ferroptosis.
sensitivity
also
governed
p53
KEAP1/NRF2
activity,
linking
ferroptosis
function
key
tumor
suppressor
pathways.
Together
these
findings
highlight
role
as
an
emerging
concept
biology
attractive
target
for
precision
medicine
discovery.
International Journal of Molecular Sciences,
Journal Year:
2019,
Volume and Issue:
20(19), P. 4968 - 4968
Published: Oct. 8, 2019
Iron,
the
fourth
most
abundant
element
in
Earth’s
crust,
is
vital
living
organisms
because
of
its
diverse
ligand-binding
and
electron-transfer
properties.
This
ability
iron
redox
cycle
as
a
ferrous
ion
enables
it
to
react
with
H2O2,
Fenton
reaction,
produce
hydroxyl
radical
(•OH)—one
reactive
oxygen
species
(ROS)
that
cause
deleterious
oxidative
damage
DNA,
proteins,
membrane
lipids.
Ferroptosis
non-apoptotic
regulated
cell
death
dependent
on
characterized
by
lipid
peroxidation.
It
triggered
when
endogenous
antioxidant
status
compromised,
leading
ROS
accumulation
toxic
damaging
structure.
Consequently,
stress
levels
cells
are
important
modulators
peroxidation
induce
this
novel
form
death.
Remedies
capable
averting
iron-dependent
peroxidation,
therefore,
lipophilic
antioxidants,
including
vitamin
E,
ferrostatin-1
(Fer-1),
liproxstatin-1
(Lip-1)
possibly
potent
bioactive
polyphenols.
Moreover,
enzymes
proteins
cascade
or
interact
pathway
ferroptosis
such
subunit
cystine/glutamate
transporter
xc−
(SLC7A11),
glutathione
peroxidase
4
(GPX4),
glutamate–cysteine
ligase
(GCLC)
metabolism
genes
transferrin
receptor
1
(TfR1)
ferroportin,
(Fpn)
heme
oxygenase
(HO-1)
ferritin
response
transcription
factor,
Nrf2.
These,
well
other
trapping
antioxidants
(RTAs),
discussed
current
review.
