Frontiers in Immunology,
Journal Year:
2022,
Volume and Issue:
13
Published: March 9, 2022
Intracerebral
hemorrhage
(ICH)
is
a
highly
fatal
disease
with
mortality
rate
of
approximately
50%.
Oxidative
stress
(OS)
prominent
cause
brain
injury
in
ICH.
Important
sources
reactive
oxygen
species
after
are
mitochondria
dysfunction,
degradated
products
erythrocytes,
excitotoxic
glutamate,
activated
microglia
and
infiltrated
neutrophils.
OS
harms
the
central
nervous
system
ICH
mainly
through
impacting
inflammation,
killing
cells
exacerbating
damage
blood
barrier.
This
review
discusses
possible
molecular
mechanisms
producing
ICH,
anti-OS
strategies
to
ameliorate
devastation
Cell Death and Disease,
Journal Year:
2020,
Volume and Issue:
11(2)
Published: Feb. 3, 2020
Abstract
Ferroptosis
is
a
new
type
of
cell
death
that
was
discovered
in
recent
years
and
usually
accompanied
by
large
amount
iron
accumulation
lipid
peroxidation
during
the
process;
occurrence
ferroptosis
iron-dependent.
Ferroptosis-inducing
factors
can
directly
or
indirectly
affect
glutathione
peroxidase
through
different
pathways,
resulting
decrease
antioxidant
capacity
reactive
oxygen
species
(ROS)
cells,
ultimately
leading
to
oxidative
death.
Recent
studies
have
shown
closely
related
pathophysiological
processes
many
diseases,
such
as
tumors,
nervous
system
ischemia-reperfusion
injury,
kidney
blood
diseases.
How
intervene
development
diseases
regulating
has
become
hotspot
focus
etiological
research
treatment,
but
functional
changes
specific
molecular
mechanisms
still
need
be
further
explored.
This
paper
systematically
summarizes
latest
progress
research,
with
on
providing
references
for
understanding
its
pathogenesis
proposing
targets
treatment
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.
Cell Death and Differentiation,
Journal Year:
2021,
Volume and Issue:
28(7), P. 2029 - 2044
Published: June 7, 2021
Tightly
orchestrated
programmed
cell
death
(PCD)
signalling
events
occur
during
normal
neuronal
development
in
a
spatially
and
temporally
restricted
manner
to
establish
the
neural
architecture
shaping
CNS.
Abnormalities
PCD
cascades,
such
as
apoptosis,
necroptosis,
pyroptosis,
ferroptosis,
associated
with
autophagy
well
unprogrammed
necrosis
can
be
observed
pathogenesis
of
various
neurological
diseases.
These
deaths
activated
response
forms
cellular
stress
(exerted
by
intracellular
or
extracellular
stimuli)
inflammatory
processes.
Aberrant
activation
pathways
is
common
feature
neurodegenerative
diseases,
amyotrophic
lateral
sclerosis
(ALS),
Alzheimer's
disease,
Parkinson's
Huntington's
resulting
unwanted
loss
cells
function.
Conversely,
inactivation
thought
contribute
brain
cancers
impact
their
therapy.
For
many
diseases
current
treatment
strategies
have
only
modest
effect,
engendering
need
for
investigations
into
origins
these
With
displaying
aberrations
pathways,
it
appears
that
agents
either
inhibit
induce
may
critical
components
future
therapeutic
strategies.
The
therapies
will
guided
preclinical
studies
animal
models
faithfully
mimic
human
disease.
In
this
review,
we
briefly
describe
processes
roles
they
play
contributing
tumorigenesis
brain.
We
also
discuss
interplay
between
distinct
cascades
disease
pharmacological
targeting
key
players
progressed
through
clinical
trials.
DNA and Cell Biology,
Journal Year:
2019,
Volume and Issue:
39(2), P. 210 - 225
Published: Dec. 6, 2019
Myocardial
ischemic
disease
affects
the
prognosis
in
perioperative
patients.
Diabetes
can
aggravate
myocardial
injury.
The
purpose
of
this
research
is
to
investigate
effect
ferroptosis
process
diabetes
mellitus
(DM)
ischemia/reperfusion
(I/R)
injury
(IRI).
Endoplasmic
reticulum
stress
(ERS)
investigated
whether
aggravates
cardiomyocytes
Rat
DM+I/R
(DIR),
cell
high
glucose
(HG),
hypoxia
reoxygenation
(H/R),
and
high-glucose
H/R
(HH/R)
models
were
established.
Ferroptosis
inhibitor
Ferrostatin-1,
agonist
Erastin,
ERS
Salubrinal,
Tunicamycin
administered.
Serum
creatine
kinase-MB
(CK-MB),
viability,
lactate
dehydrogenase
(LDH),
malondialdehyde
(MDA),
superoxide
dismutase
(SOD),
reactive
oxygen
species
(ROS),
cellular
ferrous
ion
concentration
examined.
level
ACSL4,
GPX4,
ATF4,
CHOP,
BCL-2,
BAX
was
detected.
tissue
pathological
change
detected
by
hematoxylin-eosin
staining.
Cardiac
function
monitored
invasive
hemodynamic
measurements.
Evans
Blue-triphenyltetrazolium
chloride
double
staining
used
detect
infarct
size.
In
DM+sham
(DS)
(or
HG)
I/R
H/R)
models,
injured
accompanied
increased
ERS.
Moreover,
more
serious
rat
DIR
or
HH/R
models.
Inhibition
model
could
reduce
H9c2
cells
HG,
H/R,
Erastin
stimulating
model.
Meanwhile,
inhibition
alleviate
involved
that
related
injury,
which
may
provide
a
therapeutic
regent
for
disease.
Signal Transduction and Targeted Therapy,
Journal Year:
2023,
Volume and Issue:
8(1)
Published: Sept. 21, 2023
Abstract
Ferroptosis
is
an
iron-dependent
form
of
regulated
cell
death
with
distinct
characteristics,
including
altered
iron
homeostasis,
reduced
defense
against
oxidative
stress,
and
abnormal
lipid
peroxidation.
Recent
studies
have
provided
compelling
evidence
supporting
the
notion
that
ferroptosis
plays
a
key
pathogenic
role
in
many
diseases
such
as
various
cancer
types,
neurodegenerative
disease,
involving
tissue
and/or
organ
injury,
inflammatory
infectious
diseases.
Although
precise
regulatory
networks
underlie
are
largely
unknown,
particularly
respect
to
initiation
progression
diseases,
recognized
bona
fide
target
for
further
development
treatment
prevention
strategies.
Over
past
decade,
considerable
progress
has
been
made
developing
pharmacological
agonists
antagonists
these
ferroptosis-related
conditions.
Here,
we
provide
detailed
overview
our
current
knowledge
regarding
ferroptosis,
its
pathological
roles,
regulation
during
disease
progression.
Focusing
on
use
chemical
tools
preclinical
studies,
also
summarize
recent
advances
targeting
across
growing
spectrum
ferroptosis-associated
Finally,
discuss
new
challenges
opportunities
potential
strategy
treating