Biomedicine & Pharmacotherapy,
Год журнала:
2023,
Номер
166, С. 115415 - 115415
Опубликована: Сен. 4, 2023
Iron,
as
an
essential
trace
element
for
the
organism,
is
vital
maintaining
organism's
health.
Excessive
iron
can
promote
reactive
oxygen
species
(ROS)
accumulation,
thus
damaging
cells
and
tissues.
Ferroptosis
a
novel
form
of
programmed
cell
death
distinguished
by
overload
lipid
peroxidation,
which
unique
from
autophagy,
apoptosis
necrosis,
more
studies
are
focusing
on
ferroptosis.
Recent
evidence
suggests
that
ferroptosis
associated
with
development
female
reproductive
disorders
(FRDs),
including
polycystic
ovary
syndrome
(PCOS),
premature
ovarian
insufficiency
(POI),
endometriosis
(EMs),
cancer
(OC),
preeclampsia
(PE)
spontaneous
abortion
(SA).
Pathways
genes
may
participate
in
processes
regulate
granulosa
proliferation
secretion,
oocyte
development,
reserve
function,
early
embryonic
placental
oxidative
stress.
However,
its
exact
mechanism
has
not
been
fully
revealed.
Therefore,
our
review
systematically
elaborates
occurrence
research
progress
FRDs,
view
to
providing
literature
references
clinical
targeting
-related
pathways
regulatory
factors
management
FRDs.
International Journal of Molecular Sciences,
Год журнала:
2020,
Номер
21(22), С. 8765 - 8765
Опубликована: Ноя. 20, 2020
Ferroptosis
is
a
type
of
cell
death
that
was
described
less
than
decade
ago.
It
caused
by
the
excess
free
intracellular
iron
leads
to
lipid
(hydro)
peroxidation.
Iron
essential
as
redox
metal
in
several
physiological
functions.
The
brain
one
organs
known
be
affected
homeostatic
balance
disruption.
Since
1960s,
increased
concentration
central
nervous
system
has
been
associated
with
oxidative
stress,
oxidation
proteins
and
lipids,
death.
Here,
we
review
main
mechanisms
involved
process
ferroptosis
such
peroxidation,
glutathione
peroxidase
4
enzyme
activity,
metabolism.
Moreover,
association
pathophysiology
some
neurodegenerative
diseases,
namely
Alzheimer’s,
Parkinson’s,
Huntington’s
also
addressed.
Frontiers in Pharmacology,
Год журнала:
2020,
Номер
11
Опубликована: Март 17, 2020
Ferroptosis
is
a
novel
regulated
cell
death
pattern
discovered
when
studying
the
mechanism
of
erastin-killing
RAS
mutant
tumor
cells
in
2012.
It
an
iron-dependent
programmed
pathway
mainly
caused
by
increased
redox
imbalance
but
with
distinct
biological
and
morphology
characteristics
compared
to
other
known
patterns.
associated
various
diseases
including
acute
kidney
injury,
cancer,
cardiovascular,
neurodegenerative,
hepatic
diseases.
Moreover,
activation
or
inhibition
ferroptosis
using
variety
initiators
inhibitors
can
modulate
disease
progression
animal
models.
In
this
review,
we
provide
comprehensive
analysis
ferroptosis,
its
inhibitors,
potential
role
main
metabolic
pathways
treatment
prevention
diseased
states.
We
end
review
current
knowledge
gaps
area
direction
for
future
research
on
ferroptosis.
Cell Death and Disease,
Год журнала:
2023,
Номер
14(3)
Опубликована: Март 21, 2023
Abstract
Ferroptosis
is
an
iron-dependent
regulated
cell
death
driven
by
excessive
lipid
peroxidation.
Inflammation
one
common
and
effective
physiological
event
that
protects
against
various
stimuli
to
maintain
tissue
homeostasis.
However,
the
dysregulation
of
inflammatory
responses
can
cause
imbalance
immune
system,
dysfunction
death.
Recent
studies
have
pointed
out
activation
inflammation,
including
multiple
inflammation-related
signaling
pathways,
lead
ferroptosis.
Among
related
signal
transduction
we
focused
on
five
classical
namely,
JAK-STAT,
NF-κB,
inflammasome,
cGAS-STING
MAPK
expounded
their
roles
in
To
date,
many
agents
shown
therapeutic
effects
ferroptosis-related
diseases
modulating
aforementioned
pathways
vivo
vitro.
Moreover,
regulatory
these
iron
metabolism
peroxidation
been
described
detail,
contributing
further
understanding
pathophysiological
process
Taken
together,
targeting
inflammation
will
provide
appropriate
ways
intervene
ferroptosis
diseases.
Cancers,
Год журнала:
2021,
Номер
13(5), С. 986 - 986
Опубликована: Фев. 27, 2021
It
has
been
well-established
that
cancer
cells
are
under
constant
oxidative
stress,
as
reflected
by
elevated
basal
level
of
reactive
oxygen
species
(ROS),
due
to
increased
metabolism
driven
aberrant
cell
growth.
Cancer
can
adapt
maintain
redox
homeostasis
through
a
variety
mechanisms.
The
prevalent
perception
about
ROS
is
they
one
the
key
drivers
promoting
tumor
initiation,
progression,
metastasis,
and
drug
resistance.
Based
on
this
notion,
numerous
antioxidants
aim
mitigate
stress
have
tested
for
prevention
or
treatment,
although
effectiveness
strategy
yet
be
established.
In
recent
years,
it
increasingly
appreciated
complex,
multifaceted
role
in
microenvironment
(TME),
targeted
amplify
inside
cause
destruction.
Accumulating
evidence
indicates
immunotherapies
alter
intensify
resulting
ROS-dependent
rejection.
Herein
we
review
progresses
regarding
impact
various
immune
TME,
discuss
emerging
ROS-modulating
strategies
used
combination
with
achieve
enhanced
antitumor
effects.
Antioxidants,
Год журнала:
2023,
Номер
12(9), С. 1653 - 1653
Опубликована: Авг. 22, 2023
The
liver
is
an
organ
that
particularly
exposed
to
reactive
oxygen
species
(ROS),
which
not
only
arise
during
metabolic
functions
but
also
the
biotransformation
of
xenobiotics.
disruption
redox
balance
causes
oxidative
stress,
affects
function,
modulates
inflammatory
pathways
and
contributes
disease.
Thus,
stress
implicated
in
acute
injury
pathogenesis
prevalent
infectious
or
chronic
diseases
such
as
viral
hepatitis
B
C,
alcoholic
fatty
disease,
non-alcoholic
disease
(NAFLD)
steatohepatitis
(NASH).
Moreover,
plays
a
crucial
role
progression
fibrosis,
cirrhosis
hepatocellular
carcinoma
(HCC).
Herein,
we
provide
overview
on
effects
pathophysiology
mechanisms
by
promotes
