Protein & Cell,
Journal Year:
2021,
Volume and Issue:
12(11), P. 836 - 857
Published: April 23, 2021
Ferroptosis,
an
iron-dependent
form
of
regulated
cell
death
driven
by
peroxidative
damages
polyunsaturated-fatty-acid-containing
phospholipids
in
cellular
membranes,
has
recently
been
revealed
to
play
important
role
radiotherapy-induced
and
tumor
suppression,
mediate
the
synergy
between
radiotherapy
immunotherapy.
In
this
review,
we
summarize
known
as
well
putative
mechanisms
underlying
crosstalk
ferroptosis,
discuss
interactions
ferroptosis
other
forms
induced
radiotherapy,
explore
combination
therapeutic
strategies
targeting
This
review
will
provide
frameworks
for
future
investigations
cancer
therapy.
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.
Advanced Materials,
Journal Year:
2019,
Volume and Issue:
31(51)
Published: Oct. 8, 2019
Abstract
Ferroptosis
is
a
newly
discovered
form
of
regulated
cell
death
that
the
nexus
between
metabolism,
redox
biology,
and
human
health.
Emerging
evidence
shows
potential
triggering
ferroptosis
for
cancer
therapy,
particularly
eradicating
aggressive
malignancies
are
resistant
to
traditional
therapies.
Recently,
there
has
been
great
deal
effort
design
develop
anticancer
drugs
based
on
induction.
Recent
advances
ferroptosis‐inducing
agents
at
intersection
chemistry,
materials
science,
biology
presented.
The
basis
summarized
first
highlight
feasibility
characteristics
therapy.
A
literature
review
inducers
(including
small
molecules
nanomaterials)
then
presented
delineate
their
design,
action
mechanisms,
applications.
Finally,
some
considerations
research
spotlighted,
followed
by
discussion
challenges
future
development
directions
this
burgeoning
field.
Journal of Hematology & Oncology,
Journal Year:
2020,
Volume and Issue:
13(1)
Published: Aug. 10, 2020
Abstract
In
recent
years,
cancer
immunotherapy
based
on
immune
checkpoint
inhibitors
(ICIs)
has
achieved
considerable
success
in
the
clinic.
However,
ICIs
are
significantly
limited
by
fact
that
only
one
third
of
patients
with
most
types
respond
to
these
agents.
The
induction
cell
death
mechanisms
other
than
apoptosis
gradually
emerged
as
a
new
treatment
strategy
because
tumors
harbor
innate
resistance
apoptosis.
date,
possibility
combining
two
modalities
not
been
discussed
systematically.
Recently,
few
studies
revealed
crosstalk
between
distinct
and
antitumor
immunity.
pyroptosis,
ferroptosis,
necroptosis
combined
showed
synergistically
enhanced
activity,
even
ICI-resistant
tumors.
Immunotherapy-activated
CD8+
T
cells
traditionally
believed
induce
tumor
via
following
main
pathways:
(i)
perforin-granzyme
(ii)
Fas-FasL.
identified
mechanism
which
suppress
growth
inducing
ferroptosis
provoked
review
relationship
system
activation.
Hence,
this
review,
we
summarize
knowledge
reciprocal
interaction
immunity
mechanisms,
particularly
necroptosis,
three
potentially
novel
immunogenic
death.
Because
evidence
is
derived
from
using
animal
models,
also
reviewed
related
bioinformatics
data
available
for
human
tissues
public
databases,
partially
confirmed
presence
interactions
activation
Proceedings of the National Academy of Sciences,
Journal Year:
2020,
Volume and Issue:
117(49), P. 31189 - 31197
Published: Nov. 23, 2020
Significance
This
work
demonstrates
that
oncogenic
activation
of
the
PI3K-AKT-mTOR
signaling
pathway
suppresses
ferroptosis
via
sterol
regulatory
element-binding
protein-mediated
lipogenesis,
and
inhibition
this
potentiates
cancer
therapeutic
effect
induction.
finding
unveils
mechanisms
for
regulation
provides
a
potential
approach
treating
patients
bearing
tumorigenic
mutations
in
pathway.
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.
