Journal of Hematology & Oncology,
Journal Year:
2024,
Volume and Issue:
17(1)
Published: June 6, 2024
Abstract
Ferroptosis,
an
iron-dependent
form
of
cell
death
characterized
by
uncontrolled
lipid
peroxidation,
is
governed
molecular
networks
involving
diverse
molecules
and
organelles.
Since
its
recognition
as
a
non-apoptotic
pathway
in
2012,
ferroptosis
has
emerged
crucial
mechanism
numerous
physiological
pathological
contexts,
leading
to
significant
therapeutic
advancements
across
wide
range
diseases.
This
review
summarizes
the
fundamental
mechanisms
regulatory
pathways
underlying
ferroptosis,
including
both
GPX4-dependent
-independent
antioxidant
mechanisms.
Additionally,
we
examine
involvement
various
conditions,
cancer,
neurodegenerative
diseases,
sepsis,
ischemia–reperfusion
injury,
autoimmune
disorders,
metabolic
disorders.
Specifically,
explore
role
response
chemotherapy,
radiotherapy,
immunotherapy,
nanotherapy,
targeted
therapy.
Furthermore,
discuss
pharmacological
strategies
for
modulating
potential
biomarkers
monitoring
this
process.
Lastly,
elucidate
interplay
between
other
forms
regulated
death.
Such
insights
hold
promise
advancing
our
understanding
context
human
health
disease.
Cell Death Discovery,
Journal Year:
2021,
Volume and Issue:
7(1)
Published: July 26, 2021
Abstract
Ferroptosis,
a
recently
identified
and
iron-dependent
cell
death,
differs
from
other
death
such
as
apoptosis,
necroptosis,
pyroptosis,
autophagy-dependent
death.
This
form
of
does
not
exhibit
typical
morphological
biochemical
characteristics,
including
shrinkage,
mitochondrial
fragmentation,
nuclear
condensation.
The
dysfunction
lipid
peroxide
clearance,
the
presence
redox-active
iron
well
oxidation
polyunsaturated
fatty
acid
(PUFA)-containing
phospholipids
are
three
essential
features
ferroptosis.
Iron
metabolism
peroxidation
signaling
increasingly
recognized
central
mediators
Ferroptosis
plays
an
important
role
in
regulation
oxidative
stress
inflammatory
responses.
Accumulating
evidence
suggests
that
ferroptosis
is
implicated
variety
cardiovascular
diseases
atherosclerosis,
stroke,
ischemia-reperfusion
injury,
heart
failure,
indicating
targeting
will
present
novel
therapeutic
approach
against
diseases.
Here,
we
provide
overview
features,
process,
function,
mechanisms
ferroptosis,
its
connected
relevance
to
stress,
inflammation,
Theranostics,
Journal Year:
2021,
Volume and Issue:
11(7), P. 3052 - 3059
Published: Jan. 1, 2021
Cell
death
is
an
important
component
of
the
pathophysiology
cardiovascular
disease.
An
understanding
how
cardiomyocytes
die,
and
why
regeneration
cells
in
heart
limited,
a
critical
area
study.
Ferroptosis
form
regulated
cell
that
characterized
by
iron
overload,
leading
to
accumulation
lethal
levels
lipid
hydroperoxides.
The
metabolism
iron,
lipids,
amino
acids
glutathione
tightly
controls
initiation
execution
ferroptosis.
Emerging
evidence
shows
ferroptosis
closely
associated
with
occurrence
progression
various
diseases.
In
recent
years,
has
been
found
play
roles
cardiomyopathy,
myocardial
infarction,
ischemia/reperfusion
injury,
failure.
This
article
reviews
mechanisms
which
initiated
controlled
discusses
as
novel
therapeutic
target
for
Pharmacology & Therapeutics,
Journal Year:
2023,
Volume and Issue:
244, P. 108373 - 108373
Published: March 8, 2023
Ferroptosis
is
a
type
of
regulated
cell
death
characterized
by
intracellular
accumulation
iron
and
reactive
oxygen
species,
inhibition
system
Xc-,
glutathione
depletion,
nicotinamide
adenine
dinucleotide
phosphate
oxidation
lipid
peroxidation.
Since
its
discovery
characterization
in
2012,
many
efforts
have
been
made
to
reveal
the
underlying
mechanisms,
modulating
compounds,
involvement
disease
pathways.
inducers
include
erastin,
sorafenib,
sulfasalazine
glutamate,
which,
inhibiting
prevent
import
cysteine
into
cells.
RSL3,
statins,
Ml162
Ml210
induce
ferroptosis
peroxidase
4
(GPX4),
which
responsible
for
preventing
formation
peroxides,
FIN56
withaferin
trigger
GPX4
degradation.
On
other
side,
inhibitors
ferrostatin-1,
liproxstatin-1,
α-tocopherol,
zileuton,
FSP1,
CoQ10
BH4,
interrupt
peroxidation
cascade.
Additionally,
deferoxamine,
deferiprone
N-acetylcysteine,
targeting
cellular
pathways,
also
classified
as
inhibitors.
Increased
evidence
has
established
distinct
brain
diseases,
including
Alzheimer's,
Parkinson's
Huntington's
amyotrophic
lateral
sclerosis,
multiple
Friedreich's
ataxia.
Thus,
deep
understanding
how
contributes
these
it
can
be
modulated,
open
new
window
opportunities
novel
therapeutic
strategies
targets.
Other
studies
shown
sensitivity
cancer
cells
with
mutated
RAS
induction
that
chemotherapeutic
agents
synergize
tumor
treatment.
tempting
consider
may
arise
target
mechanistic
pathway
treatment
tumors.
Therefore,
this
work
provides
an
up-to-date
review
on
molecular
mechanisms
their
diseases.
In
addition,
information
main
targets
provided.
