Ferroptosis
is
a
newly
recognized
type
of
cell
death,
which
different
from
traditional
necrosis,
apoptosis
or
autophagic
death.
However,
the
position
ferroptosis
in
lipopolysaccharide
(LPS)-induced
acute
lung
injury
(ALI)
has
not
been
explored
intensively
so
far.
In
this
study,
we
mainly
analyzed
relationship
between
and
LPS-induced
ALI.In
human
bronchial
epithelial
line,
BEAS-2B,
was
treated
with
LPS
ferrostatin-1
(Fer-1,
inhibitor).
The
viability
measured
using
CCK-8.
Additionally,
levels
malondialdehyde
(MDA),
4-hydroxynonenal
(4-HNE),
iron,
as
well
protein
level
SLC7A11
GPX4,
were
groups.
To
further
confirm
vitro
results,
an
ALI
model
induced
by
mice,
therapeutic
action
Fer-1
tissues
evaluated.The
BEAS-2B
down-regulated
treatment,
together
markers
while
MDA,
4-HNE
total
iron
increased
treatment
dose-dependent
manner,
could
be
rescued
Fer-1.
results
vivo
experiment
also
indicated
that
exerted
against
ALI,
tissues.Our
study
important
role
progression
may
become
novel
target
patients.
Cell Research,
Journal Year:
2019,
Volume and Issue:
29(5), P. 347 - 364
Published: April 4, 2019
Cells
may
die
from
accidental
cell
death
(ACD)
or
regulated
(RCD).
ACD
is
a
biologically
uncontrolled
process,
whereas
RCD
involves
tightly
structured
signaling
cascades
and
molecularly
defined
effector
mechanisms.
A
growing
number
of
novel
non-apoptotic
forms
have
been
identified
are
increasingly
being
implicated
in
various
human
pathologies.
Here,
we
critically
review
the
current
state
art
regarding
types
RCD,
including
necroptosis,
pyroptosis,
ferroptosis,
entotic
death,
netotic
parthanatos,
lysosome-dependent
autophagy-dependent
alkaliptosis
oxeiptosis.
The
in-depth
comprehension
each
these
lethal
subroutines
their
intercellular
consequences
uncover
therapeutic
targets
for
avoidance
pathogenic
loss.
Redox Biology,
Journal Year:
2019,
Volume and Issue:
23, P. 101107 - 101107
Published: Jan. 12, 2019
The
transcription
factor
nuclear
erythroid
2-related
2
(NRF2)
is
a
key
regulator
of
the
cellular
antioxidant
response,
controlling
expression
genes
that
counteract
oxidative
and
electrophilic
stresses.
Many
pathological
conditions
are
linked
to
imbalances
in
redox
homeostasis,
illustrating
important
role
defense
systems
preventing
pathogenic
effects
associated
with
accumulation
reactive
species.
In
particular,
it
becoming
increasingly
apparent
lipid
peroxides
has
an
driving
pathogenesis
multiple
disease
states.
A
example
this
recent
discovery
novel
form
cell
death
termed
ferroptosis.
Ferroptosis
iron-dependent,
peroxidation-driven
cascade
become
target
development
anti-cancer
therapies,
as
well
prevention
neurodegenerative
cardiovascular
diseases.
review,
we
will
provide
brief
overview
peroxidation,
components
involved
ferroptotic
cascade.
We
also
highlight
NRF2
signaling
pathway
mediating
peroxidation
ferroptosis,
focusing
on
established
mitigate
these
pathways,
relevance
NRF2-lipid
peroxidation-ferroptosis
axis
disease.
Journal of Hematology & Oncology,
Journal Year:
2019,
Volume and Issue:
12(1)
Published: March 29, 2019
Ferroptosis
is
a
novel
type
of
cell
death
with
distinct
properties
and
recognizing
functions
involved
in
physical
conditions
or
various
diseases
including
cancers.
The
fast-growing
studies
ferroptosis
cancer
have
boosted
perspective
for
its
usage
therapeutics.
Here,
we
review
the
current
findings
regulation
especially
focus
on
function
ncRNAs
mediating
process
ferroptotic
how
was
relation
to
other
regulated
deaths.
Aberrant
diverse
types
tissues
were
summarized,
elaborated
recent
data
about
actors
some
"conventional"
drugs
natural
compounds
as
inducers
cancer.
Finally,
deliberate
future
orientation
cells
unsettled
issues,
which
may
forward
speed
clinical
use
induction
treatment.
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.
Redox Biology,
Journal Year:
2018,
Volume and Issue:
15, P. 490 - 503
Published: Feb. 3, 2018
The
human
brain
consumes
20%
of
the
total
basal
oxygen
(O2)
budget
to
support
ATP
intensive
neuronal
activity.
Without
sufficient
O2
demands,
activity
fails,
such
that,
even
transient
ischemia
is
neurodegenerative.
While
essentiality
function
clear,
how
oxidative
stress
causes
neurodegeneration
ambiguous.
Ambiguity
exists
because
many
reasons
why
susceptible
remain
obscure.
Many
are
erroneously
understood
as
deleterious
result
adventitious
derived
free
radical
and
non-radical
species
generation.
To
understand
underpin
stress,
one
must
first
re-cast
in
a
positive
light
their
deliberate
generation
enables
achieve
critical
functions
(e.g.
synaptic
plasticity)
through
redox
signalling
(i.e.
functionality).
Using
radicals
derivatives
signal
sensitises
when
goes
awry
negative
advance
mechanistic
understanding,
we
rationalise
13
stress.
Key
include
inter
alia
unsaturated
lipid
enrichment,
mitochondria,
calcium,
glutamate,
modest
antioxidant
defence,
active
transition
metals
neurotransmitter
auto-oxidation.
We
review
RNA
oxidation
an
underappreciated
cause
complex
interplay
between
each
reason
dictates
susceptibility
dynamic
context
neural
identity
dependent
manner.
Our
discourse
sets
stage
for
investigators
interrogate
biochemical
basis
health
disease.
