Journal of Cellular Physiology,
Год журнала:
2024,
Номер
unknown
Опубликована: Дек. 5, 2024
ABSTRACT
Iron
plays
critical
roles
in
many
cellular
functions,
including
energy
production,
metabolism,
and
cell
proliferation.
However,
the
role
of
iron
maintaining
oocyte
quality
remains
unclear.
In
this
study,
DMT1
was
identified
as
a
key
transporter
during
porcine
maturation.
The
results
demonstrated
that
deficiency
led
to
aberrant
meiotic
progression,
accompanied
by
increased
gene
expression
.
Inhibition
resulted
failure
cumulus
expansion
maturation,
along
abnormal
actin
microtubule
assembly.
Furthermore,
loss
function
caused
disruption
mitochondrial
dynamics,
resulting
oxidative
stress
Ca
2+
dyshomeostasis.
Additionally,
absence
activated
PINK1/Parkin‐dependent
mitophagy
oocyte.
These
findings
suggested
played
crucial
safeguarding
protecting
against
iron‐deficiency‐induced
dysfunction
autophagy.
This
study
provided
compelling
evidence
homeostasis
were
for
capacity
Moreover,
hinted
at
potential
novel
therapeutic
target
treating
deficiency‐related
female
reproductive
disorders.
Pharmacological Research,
Год журнала:
2024,
Номер
206, С. 107258 - 107258
Опубликована: Июнь 21, 2024
Several
cardiovascular
illnesses
are
associated
with
aberrant
activation
of
cellular
pyroptosis,
ferroptosis,
necroptosis,
cuproptosis,
disulfidptosis
and
macrophage
polarisation
as
hallmarks
contributing
to
vascular
damage
abnormal
cardiac
function.
Meanwhile,
these
three
novel
forms
dysfunction
closely
related
mitochondrial
homeostasis.
Mitochondria
the
main
organelles
that
supply
energy
maintain
Mitochondrial
stability
is
maintained
through
a
series
regulatory
pathways,
such
fission,
fusion
mitophagy.
Studies
have
shown
(e.g.,
impaired
dynamics
mitophagy)
promotes
ROS
production,
leading
oxidative
stress,
which
induces
M1
phenotypic
polarisation.
Therefore,
an
in-depth
knowledge
dynamic
regulation
mitochondria
during
necessary
understand
disease
development.
This
paper
systematically
summarises
impact
changes
in
mitophagy
on
regulating
dysfunctions
promote
understanding
pathogenesis
diseases
provide
corresponding
theoretical
references
for
treating
diseases.
Oncogene,
Год журнала:
2024,
Номер
43(9), С. 650 - 667
Опубликована: Янв. 6, 2024
Transient
early
endosome
(EE)-mitochondria
interactions
can
mediate
mitochondrial
iron
translocation,
but
the
associated
mechanisms
are
still
elusive.
We
showed
that
Divalent
Metal
Transporter
1
(DMT1)
sustains
translocation
via
EE-mitochondria
in
triple-negative
MDA-MB-231,
not
luminal
A
T47D
breast
cancer
cells.
DMT1
silencing
increases
labile
pool
(LIP)
levels
and
activates
PINK1/Parkin-dependent
mitophagy
MDA-MB-231
Mitochondrial
bioenergetics
iron-associated
protein
profile
were
altered
by
rescued
re-expression.
Transcriptomic
profiles
upon
strikingly
different
between
2D
3D
culture
conditions,
suggesting
environment
context
is
crucial
for
knockout
phenotype
observed
Lastly,
vivo
lung
metastasis
assay
revealed
promoted
outgrowth
of
metastatic
nodules
both
human
murine
models
These
findings
reveal
a
DMT1-dependent
pathway
connecting
to
fitness
Molecular Metabolism,
Год журнала:
2024,
Номер
84, С. 101944 - 101944
Опубликована: Апрель 18, 2024
High-fat
diet
(HFD)
has
long
been
recognized
as
risk
factors
for
the
development
and
progression
of
ulcerative
colitis
(UC),
but
exact
mechanism
remained
elusive.
Here,
HFD
increased
intestinal
deoxycholic
acid
(DCA)
levels,
DCA
further
exacerbated
colonic
inflammation.
Transcriptome
analysis
revealed
that
triggered
ferroptosis
pathway
in
mice.
Mechanistically,
upregulated
hypoxia-inducible
factor-2α
(HIF-2α)
divalent
metal
transporter-1
(DMT1)
expression,
causing
ferrous
ions
accumulation
epithelial
cells,
which
was
reversed
by
inhibitor
ferrostatin-1.
failed
to
promote
intestine-specific
HIF-2α-null
Notably,
byak-angelicin
inhibited
DCA-induced
pro-inflammatory
pro-ferroptotic
effects
through
blocking
up-regulation
HIF-2α
DCA.
Moreover,
fat
intake
positively
correlated
with
disease
activity
UC
patients
consuming
HFD,
being
more
pronounced.
Collectively,
our
findings
demonstrated
inflammation
promoting
DCA-mediated
ferroptosis,
providing
new
insights
into
diet-related
bile
dysregulation
UC.
CNS Neuroscience & Therapeutics,
Год журнала:
2024,
Номер
30(4)
Опубликована: Апрель 1, 2024
Abstract
Objective
Neuronal
precursor
cells
expressed
developmentally
down‐regulated
4
(Nedd4)
are
believed
to
play
a
critical
role
in
promoting
the
degradation
of
substrate
proteins
and
involved
numerous
biological
processes.
However,
Nedd4
intracerebral
hemorrhage
(ICH)
remains
unknown.
This
study
aims
investigate
regulatory
ICH
model.
Methods
Male
C57BL/6J
mice
were
induced
with
ICH.
Subsequently,
levels
glutathione
peroxidase
(GPX4),
malondialdehyde
(MDA)
concentration,
iron
content,
mitochondrial
morphology,
as
well
expression
divalent
metal
transporter
1
(DMT1)
assessed
after
Furthermore,
impact
overexpression
was
evaluated
through
analyses
hematoma
area,
ferroptosis,
neurobehavioral
function.
The
mechanism
underlying
Nedd4‐mediated
DMT1
elecidated
using
immunoprecipitation
(IP)
Results
Upon
ICH,
level
brain
increased,
but
decreased
when
overexpressed
Lentivirus,
suggesting
negative
correlation
between
DMT1.
Additionally,
inhibited
it
found
that
can
interact
ubiquitinate
at
lysine
residues
6,
69,
277,
facilitating
Functional
analysis
indicated
alleviate
ferroptosis
promote
recovery
following
Conclusion
results
demonstrated
occurs
via
Nedd4/DMT1
pathway
during
potential
valuable
target
inhibit
for
treatment
This
study
aims
to
investigate
the
role
and
mechanism
of
p-hydroxyl
cinnamaldehyde
(CMSP)
in
triggering
ferroptosis
small
cell
lung
cancer
(SCLC)
cells.
The
impact
CMSP
on
H1688
SW1271
cells
was
assessed
through
experiments
biological
information
analysis.
Moreover,
expression
heme
oxygenase
1
(HMOX1)
SCLC
tissue
examined.
Following
treatment,
a
concentration-dependent
increase
death
observed,
differentially
expressed
genes
were
found
be
associated
with
ferroptosis.
notably
facilitated
events,
such
as
elevated
levels
reactive
oxygen
species
(ROS),
Fe2+,
malondialdehyde
(MDA),
transferrin
receptor
(TFR1),
divalent
metal
transporter
(DMT1),
decreased
glutathione
(GSH),
solute
carrier
family
7
member
11
(SLC7A11),
peroxidase
4
(GPX4).
Furthermore,
promoted
mitochondrial
dysfunction,
manifested
reduced
volume,
increased
membrane
density,
ROS,
potential.
Consistently,
mitochondrial-targeted
antioxidant
Mito-TEMPO
reversed
CMSP-induced
Expression
HMOX1
gene
markedly
under
while
lower
observed
compared
adjacent
tissue.
triggers
dysfunction
via
activation,
leading
cells,
underscoring
its
potential
therapeutic
agent
for
SCLC.
