Abstract
During
uterine
spiral
artery
remodeling,
vascular
smooth
muscle
cells
(VSMCs)
become
disorganized
and
undergo
phenotypic
switching
from
a
contractile
to
more
synthetic
phenotype.
We
have
previously
reported
that
natural
killer
induce
this
VSMC
by
secreting
angiopoietin‐2
(Ang‐2).
Here,
we
identified
the
specific
mechanisms
which
Ang‐2
plays
role
in
phenomenon.
VSMCs
isolated
human
umbilical
arteries
were
used
as
an
vitro
model
investigate
of
switching.
Human
decidua
tissue
preeclamptic
control
pregnancies
was
collected
compare
expression
levels
related
proteins.
induced
phenotype
evidenced
decreased
marker
expression,
increased
proliferation
migration,
altered
cytoskeleton.
expressed
integrin
β6
interacted
directly
with
phosphorylation
FAK
(S910
Y397),
AKT
(S473),
mTOR
(S2448).
Knockdown
recovered
calponin
loss
resulted
lower
EZH2
abundance.
Inhibition
both
attenuated
Ang‐2‐induced
inhibition
LC3
II/LC3
I
ratio
ATG7
proliferation.
Lipid
peroxidation
ferrostatin‐1
or
IL‐8
receptor
antagonist
navarixin
inhibited
migration.
secretion
significantly
lipid
inhibition.
In
decidua,
there
unremodeled
arteries,
abundance
dysregulated.
dysregulation
may
disrupt
remodeling
contribute
preeclampsia.
be
novel
therapeutic
target
for
treatment
pregnancy
complications
affected
incomplete
remodeling.
Biomolecules,
Год журнала:
2024,
Номер
14(2), С. 142 - 142
Опубликована: Янв. 23, 2024
Regulated
cell
death
(RCD)
represents
a
distinct
mode
of
demise,
differing
from
accidental
(ACD),
characterized
by
specific
signaling
cascades
orchestrated
diverse
biomolecules.
The
regular
process
plays
crucial
role
in
upholding
internal
homeostasis,
acting
as
safeguard
against
biological
or
chemical
damage.
Nonetheless,
programmed
deaths
have
the
potential
to
activate
an
immune–inflammatory
response,
potentially
contributing
diseases
enlisting
immune
cells
and
releasing
pro-inflammatory
factors.
Endometriosis,
prevalent
gynecological
ailment,
remains
incompletely
understood
despite
substantial
progress
unraveling
associated
pathways.
Its
complexity
is
intricately
tied
dysregulation
inflammatory
responses,
with
various
RCD
processes
such
apoptosis,
autophagic
death,
pyroptosis,
ferroptosis
implicated
its
development.
Notably,
limited
research
explores
association
between
endometriosis
pathways
like
pyroptosis
cuproptosis.
exploration
regulated
context
holds
tremendous
for
further
advancements.
This
article
thoroughly
reviews
molecular
mechanisms
governed
their
implications
endometriosis.
A
comprehensive
understanding
mechanism
has
catalyze
development
promising
therapeutic
strategies
chart
course
future
directions
field.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(12), С. 6298 - 6298
Опубликована: Июнь 7, 2024
Endometriosis
in
half
of
affected
women
is
closely
related
to
problems
with
fertility.
Endometriosis-associated
infertility
caused
by
a
wide
range
abnormalities
affecting
the
female
reproductive
tract,
from
oocyte
quality
impairment
disturbances
eutopic
endometrium
or
mechanical
resulting
disease
progression.
Since
supportive
antioxidant
therapies,
addition
surgical
treatment
assisted
techniques
(ARTs),
have
overall
been
proven
be
effective
tools
endometriosis
management,
objective
our
review
was
analyze
role
substances,
including
vitamins,
micronutrients,
N-acetylcysteine
(NAC),
curcumin,
melatonin,
and
resveratrol,
endometriosis-related
infertility.
Most
these
substances
alleviate
systemic
oxidant
predominance,
which
has
expressed
through
decreased
oxidative
stress
(OS)
markers
enhanced
antioxidative
defense.
In
addition,
we
demonstrated
that
predominant
effect
aforementioned
inhibition
development
endometriotic
lesions
as
well
suppression
pro-inflammatory
molecules.
Although
can
undoubtedly
conclude
antioxidants
are
beneficial
fertility
support,
further
studies
explaining
detailed
pathways
their
action
needed.
Medicine,
Год журнала:
2024,
Номер
103(11), С. e37421 - e37421
Опубликована: Март 15, 2024
Endometriosis
(EMT)
a
common
gynecological
condition
in
women,
an
inflammatory
disease
characterized
by
the
presence
of
endometrial
tissue
on
organs
and
tissues
pelvis,
is
mainly
associated
with
chronic
pelvic
pain
infertility.
As
etiology
has
not
been
fully
elucidated,
current
treatment
limited
to
surgery,
hormones
painkillers,
more
side
effects
difficulty
achieving
long-term
relief.
Oxidative
stress
manifests
itself
as
overproduction
reactive
oxygen
species,
which
integral
impact
pathology
female
reproductive
disorders.
In
this
review,
we
evaluate
mechanisms
iron
overload-induced
oxidative
ferroptosis
EMT
their
pathophysiological
implications.
Frontiers in Pharmacology,
Год журнала:
2022,
Номер
13
Опубликована: Сен. 2, 2022
Endometriosis
(EMs)
is
defined
as
the
presence
of
tissue
somewhat
resembling
endometrial
glands
and
stroma
outside
uterus;
retrograded
endometrium
grows
in
peritoneal
cavity
elicits
fibrosis.
Ferroptosis
a
recently
discovered
form
programmed
cell
death,
which
iron-dependent.
The
induction
ferroptosis
has
been
found
to
participate
However,
relationship
between
EMs
fibrosis
remains
unknown.
In
this
study,
we
confirmed
that
iron
content
ectopic
stromal
ovarian
significantly
increased.
We
explored
role
iron-induced
pathogenesis
for
first
time.
tissues
was
enhanced
than
eutopic
tissues.
Furthermore,
performed
vivo
drug
screening
induced
by
ferric
ammonium
citrate
(FAC)
could
aggravate
To
clarify
mechanism
process,
composition
human
uterine
characterized.
Fibroblast-specific
protein-1
used
fibroblasts,
smooth
muscle
actin
alpha
myofibroblasts,
platelet-derived
growth
factor
receptor
beta
(CD140b)
mesenchymal
cells
(MSCs).
results
demonstrated
percentage
myofibroblasts
higher
portion
MSCs
lower
those
endometrium.
Moreover,
proportion
decreased
increased
considerably
after
FAC
treatment
vitro.
disruption
intracellular
levels
or
via
chelation
deferoxamine
mesylate
inhibitor
ferrostatin-1
reverse
indicating
plays
vital
Considering
accumulation
can
feed
Fenton
reaction
generate
unquenchable
amounts
free
radicals,
causing
damage
thereby
contributing
fibrosis,
validated
underlying
excess
facilitate
fibrotic
responses.
Collectively,
these
data
provide
evidence
supernumerary
key
regulator
promoting
inducing
The American Journal of Chinese Medicine,
Год журнала:
2025,
Номер
unknown, С. 1 - 24
Опубликована: Март 27, 2025
Endometriosis
(EMS)
is
a
chronic,
estrogen-dependent
inflammatory
disease
affecting
5–10%
of
women
reproductive
age,
characterized
by
the
growth
endometrial
tissue
on
outside
uterus.
The
dysregulation
iron
metabolism
leads
to
accumulation
ions
at
lesion
sites,
resulting
in
oxidative
stress
and
pro-inflammatory
responses
that
promote
progression
EMS.
mechanisms
underlying
ferroptosis
EMS
primarily
involve
accumulation,
lipid
peroxidation,
loss
glutathione
peroxidase
4
activity.
These
confer
resistance
within
ectopic
tissues
facilitate
cell
survival
proliferation.
Traditional
Chinese
medicine
(TCM)
has
demonstrated
therapeutic
potential
for
modulating
ferroptosis.
Studies
have
shown
TCM
monomers
may
regulate
transport
proteins
anti-oxidant
defense
mechanisms.
formulas
employ
distinct
treatment
strategies
depending
stage
EMS:
early
stages,
they
control
growth,
whereas
later
inhibit
reduce
inflammation
order
improve
health
slow
progression.
This
study
provides
new
perspective
management
summarizing
role
its
pathological
reviewing
findings
use
regulating
Oxidative Medicine and Cellular Longevity,
Год журнала:
2022,
Номер
2022, С. 1 - 20
Опубликована: Ноя. 24, 2022
Hepatocellular
carcinoma
(HCC)
is
a
prevalent
malignant
tumor
worldwide.
Ferroptosis
emerging
as
an
effective
target
for
treatment
it
has
been
shown
to
potentiate
cell
death
in
some
malignancies.
However,
remains
unclear
whether
histone
phosphorylation
events,
epigenetic
mechanism
that
regulates
transcriptional
expression,
are
involved
ferroptosis.
Our
study
found
supplementation
with
anisomycin,
agonist
of
p38
mitogen-activated
protein
kinase
(MAPK),
induced
ferroptosis
HCC
cells,
and
the
H3
on
serine
10
(p-H3S10)
was
participated
anisomycin-induced
To
investigate
anticancer
effects
anisomycin-activated
MAPK
HCC,
we
analyzed
viability,
colony
formation,
death,
migration
Hep3B
HCCLM3
cells.
The
results
showed
anisomycin
could
significantly
suppress
formation
induce
death.
hallmarks
ferroptosis,
such
abnormal
accumulation
iron
elevated
levels
lipid
peroxidation
malondialdehyde,
were
detected
confirm
ability
promote
Furthermore,
coincubation
SB203580,
inhibitor
activated
MAPK,
partially
rescued
And
p-p38
p-H3S10
successively
increased
by
treatment.
relationship
between
revealed
ChIP
sequencing.
reverse
transcription
PCR
immunofluorescence
NCOA4
upregulated
both
mRNA
after
C11-BODIPY
staining,
reactive
oxygen
species
reduced
knockdown.
In
conclusion,
promoted
cells
through
H3S10
phosphorylation.
Diagnostics,
Год журнала:
2023,
Номер
13(11), С. 1926 - 1926
Опубликована: Май 31, 2023
To
date,
the
development
of
therapy
for
endometriosis
and
disease-related
infertility
remains
a
major
challenge.
Iron
overload
caused
by
periodic
bleeding
is
hallmark
endometriosis.
Ferroptosis
an
iron-
lipid-reactive
oxygen
species-dependent
type
programmed
cell
death
that
distinct
from
apoptosis,
necrosis,
autophagy.
This
review
summarizes
current
understanding
future
directions
research
treatment
infertility,
with
main
focus
on
molecular
basis
ferroptosis
in
endometriotic
granulosa
cells.
Papers
published
between
2000
2022
PubMed
Google
Scholar
databases
were
included
this
review.
Emerging
evidence
suggests
closely
linked
to
pathophysiology
Endometriotic
cells
are
characterized
resistance,
whereas
remain
highly
susceptible
ferroptosis,
suggesting
regulation
utilized
as
interventional
target
into
infertility.
New
therapeutic
strategies
urgently
needed
efficiently
kill
while
protecting
An
analysis
pathway
vitro,
vivo,
animal
enhances
our
pathogenesis
disease.
Here,
we
discuss
role
modulators
approach
potential
novel
Communications Biology,
Год журнала:
2024,
Номер
7(1)
Опубликована: Янв. 5, 2024
Abstract
Mitochondrial
transcription
termination
factor
3
(MTERF3)
negatively
regulates
mitochondrial
DNA
transcription.
However,
its
role
in
hepatocellular
carcinoma
(HCC)
progression
remains
elusive.
Here,
we
investigate
the
expression
and
function
of
MTERF3
HCC.
is
overexpressed
HCC
tumor
tissues
higher
positively
correlates
with
poor
overall
survival
patients.
Knockdown
induces
dysfunction,
S-G2/M
cell
cycle
arrest
apoptosis,
resulting
proliferation
inhibition.
In
contrast,
overexpression
promotes
proliferation.
Mechanistically,
dysfunction
induced
by
knockdown
ROS
accumulation,
activating
p38
MAPK
signaling
pathway
to
suppress
conclusion,
accumulation
inhibits
via
suggesting
a
promising
target