Nature Communications,
Journal Year:
2022,
Volume and Issue:
13(1)
Published: June 27, 2022
Abstract
Immunogenic
cell
death
significantly
contributes
to
the
success
of
anti-cancer
therapies,
but
immunogenicity
different
modalities
widely
varies.
Ferroptosis,
a
form
that
is
characterized
by
iron
accumulation
and
lipid
peroxidation,
has
not
yet
been
fully
evaluated
from
this
perspective.
Here
we
present
an
inducible
model
ferroptosis,
distinguishing
three
phases
in
process—‘initial’
associated
with
‘intermediate’
correlated
ATP
release
‘terminal’
recognized
HMGB1
loss
plasma
membrane
integrity—that
serves
as
tool
study
immune
responses
ferroptotic
cancer
cells.
Co-culturing
cells
dendritic
(DC),
reveals
‘initial’
decrease
maturation
DC,
are
poorly
engulfed,
dampen
antigen
cross-presentation.
DC
loaded
ferroptotic,
contrast
necroptotic,
fail
protect
against
tumor
growth.
Adding
immunogenic
apoptotic
dramatically
reduces
their
prophylactic
vaccination
potential.
Our
thus
shows
ferroptosis
negatively
impacts
presenting
hence
adaptive
response,
which
might
hinder
therapeutic
applications
induction.
Cell Research,
Journal Year:
2020,
Volume and Issue:
31(2), P. 107 - 125
Published: Dec. 2, 2020
Abstract
Cell
death
can
be
executed
through
different
subroutines.
Since
the
description
of
ferroptosis
as
an
iron-dependent
form
non-apoptotic
cell
in
2012,
there
has
been
mounting
interest
process
and
function
ferroptosis.
Ferroptosis
occur
two
major
pathways,
extrinsic
or
transporter-dependent
pathway
intrinsic
enzyme-regulated
pathway.
is
caused
by
a
redox
imbalance
between
production
oxidants
antioxidants,
which
driven
abnormal
expression
activity
multiple
redox-active
enzymes
that
produce
detoxify
free
radicals
lipid
oxidation
products.
Accordingly,
precisely
regulated
at
levels,
including
epigenetic,
transcriptional,
posttranscriptional
posttranslational
layers.
The
transcription
factor
NFE2L2
plays
central
role
upregulating
anti-ferroptotic
defense,
whereas
selective
autophagy
may
promote
ferroptotic
death.
Here,
we
review
current
knowledge
on
integrated
molecular
machinery
describe
how
dysregulated
involved
cancer,
neurodegeneration,
tissue
injury,
inflammation,
infection.
Autophagy,
Journal Year:
2020,
Volume and Issue:
17(9), P. 2054 - 2081
Published: Aug. 19, 2020
Ferroptosis
is
an
iron-dependent,
non-apoptotic
form
of
regulated
cell
death
caused
by
lipid
peroxidation,
which
controlled
integrated
oxidation
and
antioxidant
systems.
The
iron-containing
enzyme
lipoxygenase
the
main
promoter
ferroptosis
producing
hydroperoxides,
its
function
relies
on
activation
ACSL4-dependent
biosynthesis.
In
contrast,
selenium-containing
GPX4
currently
recognized
as
a
central
repressor
ferroptosis,
activity
depends
glutathione
produced
from
cystine-glutamate
antiporter
SLC7A11.
Many
metabolic
(especially
involving
iron,
lipids,
amino
acids)
degradation
pathways
(macroautophagy/autophagy
ubiquitin-proteasome
system)
orchestrate
complex
ferroptotic
response
through
direct
or
indirect
regulation
iron
accumulation
peroxidation.
Although
detailed
mechanism
membrane
injury
during
remains
mystery,
ESCRT
III-mediated
plasma
repair
can
make
cells
resistant
to
ferroptosis.
Here,
we
review
recent
rapid
progress
in
understanding
molecular
mechanisms
focus
epigenetic,
transcriptional,
posttranslational
this
process.Abbreviations:
2ME:
beta-mercaptoethanol;
α-KG:
α-ketoglutarate;
ccRCC:
clear
renal
carcinoma;
EMT:
epithelial-mesenchymal
transition;
FAO:
fatty
acid
beta-oxidation;
GSH:
glutathione;
MEFs:
mouse
embryonic
fibroblasts;
MUFAs:
monounsaturated
acids;
NO:
nitric
oxide;
NOX:
NADPH
oxidase;
PPP:
pentose
phosphate
pathway;
PUFA:
polyunsaturated
acid;
RCD:
death;
RNS:
reactive
nitrogen
species;
ROS:
oxygen
RTAs:
radical-trapping
antioxidants;
UPS:
system;
UTR:
untranslated
region.
Signal Transduction and Targeted Therapy,
Journal Year:
2021,
Volume and Issue:
6(1)
Published: Feb. 3, 2021
Abstract
Ferroptosis
is
an
iron-dependent
cell
death,
which
different
from
apoptosis,
necrosis,
autophagy,
and
other
forms
of
death.
The
process
ferroptotic
death
defined
by
the
accumulation
lethal
lipid
species
derived
peroxidation
lipids,
can
be
prevented
iron
chelators
(e.g.,
deferiprone,
deferoxamine)
small
lipophilic
antioxidants
ferrostatin,
liproxstatin).
This
review
summarizes
current
knowledge
about
regulatory
mechanism
ferroptosis
its
association
with
several
pathways,
including
iron,
lipid,
cysteine
metabolism.
We
have
further
discussed
contribution
to
pathogenesis
diseases
such
as
cancer,
ischemia/reperfusion,
various
neurodegenerative
Alzheimer’s
disease
Parkinson’s
disease),
evaluated
therapeutic
applications
inhibitors
in
clinics.
Biomedicine & Pharmacotherapy,
Journal Year:
2020,
Volume and Issue:
127, P. 110108 - 110108
Published: March 29, 2020
Ferroptosis
is
a
newly
discovered
type
of
cell
death
triggered
by
intracellular
phospholipid
peroxidation
that
morphologically,
biologically
and
genetically
distinct
from
other
types
death.
classified
as
regulated
necrosis
more
immunogenic
than
apoptosis.
To
date,
compelling
evidence
indicates
ferroptosis
plays
an
important
role
in
inflammation,
several
antioxidants
functioning
inhibitors
have
been
shown
to
exert
anti-inflammatory
effects
experimental
models
certain
diseases.
Our
review
provides
overview
the
link
between
inflammation;
better
understanding
mechanisms
underlying
inflammation
may
hasten
development
promising
therapeutic
strategies
involving
address
inflammation.
The Journal of Experimental Medicine,
Journal Year:
2021,
Volume and Issue:
218(6)
Published: May 12, 2021
Ferroptosis
is
a
type
of
regulated
necrosis
that
triggered
by
combination
iron
toxicity,
lipid
peroxidation,
and
plasma
membrane
damage.
The
upstream
inducers
ferroptosis
can
be
divided
into
two
categories
(biological
versus
chemical)
activate
major
pathways
(the
extrinsic/transporter
the
intrinsic/enzymatic
pathways).
Excessive
or
deficient
ferroptotic
cell
death
implicated
in
growing
list
physiological
pathophysiological
processes,
coupled
to
dysregulated
immune
response.
This
review
focuses
on
new
discoveries
related
how
cells
their
spilled
contents
shape
innate
adaptive
immunity
health
disease.
Understanding
immunological
characteristics
activity
not
only
illuminates
an
intersection
between
but
may
also
lead
development
novel
treatment
approaches
for
immunopathological
diseases.
Frontiers in Neuroscience,
Journal Year:
2020,
Volume and Issue:
14
Published: April 21, 2020
Ferroptosis
is
a
kind
of
regulated
cell
death
(RCD)
caused
by
the
redox
state
disorder
intracellular
microenvironment
controlled
glutathione
peroxidase
4
(GPX4),
which
inhibited
iron
chelators
and
lipophilic
antioxidants.
In
addition
to
classical
regulatory
mechanisms,
new
factors
for
ferroptosis
have
been
discovered
in
recent
years,
such
as
P53
pathway,
ATF3/4
Beclin
1
(BECN1)
some
non-coding
RNA.
closely
related
cancer
treatment,
neurodegenerative
diseases,
ischemia-reperfusion
organ,
neurotoxicity,
other
particular,
field
diseases
treatment
has
aroused
people's
interest.
The
nuclear
factor
E2
2
(Nrf2/NFE2L2)
proved
play
key
role
neurodegeneration
disease
regulation.
promotes
progression
while
expression
Nrf2
its
target
genes
(Ho-1,
Nqo-1,
Trx)
declined
with
aging,
therefore,
there
still
insufficient
evidence
networks
diseases.
this
review,
we
will
provide
brief
overview
well
an
emphasis
on
mechanism
regulating
ferroptosis.
We
also
highlight
during
process
investigate
theoretical
basis
further
research
relationship
between
treatment.
