Cell chemical biology,
Journal Year:
2020,
Volume and Issue:
27(4), P. 436 - 447
Published: April 1, 2020
Ferroptosis
is
a
non-apoptotic
mode
of
regulated
cell
death
that
iron
and
lipid
peroxidation
dependent.
As
new
mechanistic
insight
into
ferroptotic
effectors
how
they
are
in
different
disease
contexts
uncovered,
our
understanding
the
physiological
pathological
relevance
this
continues
to
grow.
Along
these
lines,
host
pharmacological
modulators
pathway
have
been
identified,
targeting
proteins
involved
homeostasis;
generation
reduction
peroxides;
or
cystine
import
glutathione
metabolism.
Also,
note,
many
components
ferroptosis
cascade
target
genes
transcription
factor
nuclear
erythroid
2-related
2
(NRF2),
indicating
its
critical
role
mediating
response.
In
review,
we
discuss
vitro,
vivo,
clinical
evidence
disease,
including
brief
discussion
upstream
mediators
cascade,
NRF2,
treat
ferroptosis-driven
diseases.
Cell Death and Differentiation,
Journal Year:
2018,
Volume and Issue:
25(3), P. 486 - 541
Published: Jan. 23, 2018
Over
the
past
decade,
Nomenclature
Committee
on
Cell
Death
(NCCD)
has
formulated
guidelines
for
definition
and
interpretation
of
cell
death
from
morphological,
biochemical,
functional
perspectives.
Since
field
continues
to
expand
novel
mechanisms
that
orchestrate
multiple
pathways
are
unveiled,
we
propose
an
updated
classification
subroutines
focusing
mechanistic
essential
(as
opposed
correlative
dispensable)
aspects
process.
As
provide
molecularly
oriented
definitions
terms
including
intrinsic
apoptosis,
extrinsic
mitochondrial
permeability
transition
(MPT)-driven
necrosis,
necroptosis,
ferroptosis,
pyroptosis,
parthanatos,
entotic
death,
NETotic
lysosome-dependent
autophagy-dependent
immunogenic
cellular
senescence,
mitotic
catastrophe,
discuss
utility
neologisms
refer
highly
specialized
instances
these
processes.
The
mission
NCCD
is
a
widely
accepted
nomenclature
in
support
continued
development
field.
Proceedings of the National Academy of Sciences,
Journal Year:
2019,
Volume and Issue:
116(7), P. 2672 - 2680
Published: Jan. 28, 2019
Significance
Nonapoptotic
cell
death-induced
tissue
damage
has
been
implicated
in
a
variety
of
diseases,
including
neurodegenerative
disorder,
inflammation,
and
stroke.
In
this
study,
we
demonstrate
that
ferroptosis,
newly
defined
iron-dependent
death,
mediates
both
chemotherapy-
ischemia/reperfusion-induced
cardiomyopathy.
RNA-sequencing
analysis
revealed
up-regulation
heme
oxygenase
1
by
doxorubicin
as
major
mechanism
ferroptotic
As
result,
degrades
releases
free
iron
cardiomyocytes,
which
turn
leads
to
generation
oxidized
lipids
the
mitochondria
membrane.
Most
importantly,
chelation
therapy
pharmacologically
blocking
ferroptosis
could
significantly
alleviate
cardiomyopathy
mice.
These
findings
suggest
targeting
strategy
for
treating
deadly
heart
disease.
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.
Cell Death and Differentiation,
Journal Year:
2019,
Volume and Issue:
26(11), P. 2284 - 2299
Published: Feb. 8, 2019
Ferroptosis
is
a
recently
identified
form
of
regulated
cell
death
defined
by
the
iron-dependent
accumulation
lipid
reactive
oxygen
species.
has
been
studied
in
various
diseases
such
as
cancer,
Parkinson's
disease,
and
stroke.
However,
exact
function
mechanism
ferroptosis
ischemia/reperfusion
(I/R)
injury,
especially
intestine,
remains
unknown.
Considering
unique
conditions
required
for
ferroptosis,
we
hypothesize
that
ischemia
promotes
immediately
after
intestinal
reperfusion.
In
contrast
to
conventional
strategies
employed
I/R
studies,
focused
on
ischemic
phase.
Here
verified
assessing
proferroptotic
changes
along
with
protein
peroxidation
levels
during
The
inhibition
liproxstatin-1
ameliorated
I/R-induced
injury.
Acyl-CoA
synthetase
long-chain
family
member
4
(ACSL4),
which
key
enzyme
regulates
composition,
shown
contribute
execution
but
its
role
needs
clarification.
present
study,
used
rosiglitazone
(ROSI)
siRNA
inhibit
ischemia/hypoxia-induced
ACSL4
vivo
vitro.
results
demonstrated
before
reperfusion
protected
against
death.
Further
investigation
revealed
special
1
(Sp1)
was
crucial
transcription
factor
increased
binding
promoter
region.
Collectively,
this
study
demonstrates
closely
associated
critical
lethal
process.
Sp1
an
important
promoting
expression.
These
suggest
effective
mechanistic
approach
injury
prevention
treatment.