Cell Death Discovery,
Journal Year:
2025,
Volume and Issue:
11(1)
Published: Feb. 5, 2025
Abstract
Traumatic
brain
injury
(TBI)
is
one
of
the
leading
causes
disability
and
mortality,
which
was
classified
as
low-altitude
TBI
high-altitude
TBI.
A
large
amount
literature
shows
that
associated
with
more
severe
neurological
impairments
higher
mortality
rates
compared
to
TBI,
due
special
environment
hypoxia.
However,
role
hypoxia
in
pathogenesis
remains
unclear.
In
order
deeply
investigate
this
scientific
issue,
we
constructed
a
hypoxic
model
at
different
altitudes
used
animal
behavioral
assessments
(Modified
severity
score,
rotarod
test,
elevated
plus
maze
test)
well
histopathological
analyses
(brain
gross
specimens,
water
content,
Evans
blue
inducible
factor-1α,
Hematoxylin-Eosin
staining
ROS
detection)
reveal
its
underlying
principles
characteristics.
We
found
altitude,
TBI-induced
deficits
were
changes
significant.
Single-nuclear
RNA
sequencing
subsequently
employed
further
differential
gene
expression
profiles
significant
increase
ferroptosis
astrocytes
cases
those
Analyzing
transcription
factors
depth,
Bach1
plays
crucial
regulating
key
molecules
induce
following
Down-regulation
can
effectively
alleviate
mice.
conclusion,
may
significantly
enhance
aggravate
by
up-regulating
expression.
Our
study
provides
theoretical
foundation
for
understanding
mechanism
targeted
intervention
therapy.
Brain Behavior and Immunity,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 1, 2025
Various
forms
of
neuronal
death
contribute
to
neurological
injury
after
traumatic
brain
(TBI),
leading
irreversible
deficits.
Among
these,
ferroptosis
is
a
form
regulated
cell
characterized
by
the
accumulation
iron-dependent
lipid
hydroperoxides
and
induced
incorporation
polyunsaturated
fatty
acids
(PUFAs)
into
cellular
membranes.
Adiponectin
(APN),
cytokine
secreted
adipocytes,
have
showed
neuroprotective
effects
binding
adiponectin
receptors
(AdipoRs),
which
are
widely
expressed
in
central
nervous
system.
However,
role
TBI
APN-AdipoRs
signaling
remains
unexplored.
Our
clinical
analysis
revealed
significant
correlation
between
serum
levels
APN
6-month
outcomes
patients.
Subsequent
studies
confirmed
that
TBI-induced
was
more
pronounced
knockout
mice
compared
wild-type
mice,
while
additional
receptor
agonist
(AdipoRon)
treatment
significantly
mitigated
ferroptosis.
Furthermore,
AdipoR1
knockdown
diminished
protective
AdipoRon
against
erastin-induced
primary
neurons.
Correspondingly,
neuron-specific
conditional
(AdipoR1CKO)
neurons
were
susceptible
TBI,
increased
edema
lesion
volume,
exacerbated
Mechanically,
activation
APN-AdipoR1
promoted
adenosine
monophosphate
activated
protein
kinase
(AMPK)
-mediated
phosphorylation
acetyl-CoA
carboxylase-1
(ACC1),
thus
suppressed
PUFAs
biosynthesis,
determines
theferroptosissensitivity
Taken
together,
these
findings
provided
compelling
evidence
for
inhibiting
AMPK-ACC1.
Cell Death and Disease,
Journal Year:
2025,
Volume and Issue:
16(1)
Published: March 4, 2025
Abstract
Neuronal
cell
death
is
a
causative
process
in
traumatic
brain
injury
(TBI)-induced
structural
and
functional
impairment
of
the
central
nervous
system.
However,
upstream
trigger
TBI-induced
neuronal
loss
underlying
molecular
pathways
remain
unclear.
Zipper-interacting
protein
kinase
(ZIPK)
has
been
shown
to
be
upregulated
Alzheimer’s
disease
ischemic
stroke
play
role
cellular
apoptosis,
while
its
pathological
significance
TBI
not
reported.
Herein,
we
discovered
for
first
time
that
ZIPK
expression
was
markedly
elevated
neurons
after
caused
massive
apoptosis
peri-contusional
regions.
Zipk
haploinsufficiency
antagonized
reversed
several
typical
neuropathological
changes
induced
by
TBI.
Mechanistically,
found
affected
viability
modulating
effector
domain-containing
DNA
binding
(DEDD)
caspase-3
pathway.
Specifically,
could
bind
phosphorylate
DEDD
at
S9
residue,
thus
enhancing
stability
DEDD,
leading
activation
caspase-3-mediated
apoptotic
cascade
neurons.
The
rescue
downregulation
effectively
alleviated
behavioral
deficits
preserving
motor
cognitive
abilities
vivo,
supporting
decisive
dysregulation
TBI-associated
dysfunctions
survival.
Furthermore,
pharmacological
suppression
activity
specific
inhibitor
prior
protected
from
injury-induced
degeneration
vitro
vivo
preventing
upregulation
activation.
In
conclusion,
our
data
reveal
essential
contribution
through
DEDD/caspase-3
cascade,
suggest
potential
targeting
as
an
effective
strategy
treating
TBI-related
neuropathologies.
The Journal of Nutritional Biochemistry,
Journal Year:
2025,
Volume and Issue:
unknown, P. 109888 - 109888
Published: March 1, 2025
Iron
is
essential
in
various
physiological
processes,
but
its
accumulation
leads
to
oxidative
stress
and
cell
damage,
thus
iron
homeostasis
has
be
tightly
regulated.
Ferroptosis
an
iron-dependent
non-apoptotic
regulated
death
characterized
by
overload
ROS
accumulation.
Mitochondria
are
organelles
playing
a
crucial
role
metabolism
involved
ferroptosis.
MitoNEET,
protein
of
mitochondrial
outer
membrane,
key
element
this
process.
Ferroptosis,
altering
levels
several
metabolically
active
organs,
linked
non-communicable
diseases.
For
example,
the
liver
hepatic
fibrosis
cirrhosis,
accelerating
NAFLD
progression,
muscle
cells
contributes
damage
leading
sarcopenia,
brain
associated
neurodegeneration.
The
aim
review
investigate
intricate
balance
regulation
focusing
on
mitochondria
stress,
analyzing
ferroptosis
implications
health
disease.
Poultry Science,
Journal Year:
2024,
Volume and Issue:
103(6), P. 103674 - 103674
Published: March 16, 2024
Microplastics
biological
toxicity,
environmental
persistence
and
chemicals
have
been
paid
widespread
attention.
exposed
to
chicken
spleen
injury
of
the
specific
mechanism
is
unclear.
Thus,
we
randomly
assigned
chickens
4
groups:
C
(normal
diet),
L-MPs
(1
mg/L),
M-MPs
(10
H-MPs
(100
assessed
damage
after
42
d
exposure.
Morphologically,
boundary
between
red
white
pulp
was
blurred,
along
with
expansion
pulp.
It
further
speculated
that
microplastics
induced
mitochondrial
dynamic
homeostasis
(Drp1
upgraded,
Mfn1,
Mfn2,
OPA1
reduced),
provoked
apoptotic
pathway
(Bcl-2/Bax
decreased,
cytc,
caspase3,
caspase9
raised),
resulting
in
redox
imbalance
lipid
peroxide
accumulation
(MDA
increased,
CAT,
GSH,
T-AOC
plummeted),
stimulated
ferroptosis
(FTH1,
GPX4,
SLC7A11
decreased).
Here
explored
impact
polystyrene
on
spleen,
as
well
programmed
death
(apoptosis
ferroptosis)
involved,
regulative
role
mitochondria
this
process.
This
could
be
significant
importance
bridging
gap
laboratory
research
microplastics-induced
chicken.
Open Medicine,
Journal Year:
2025,
Volume and Issue:
20(1)
Published: Jan. 1, 2025
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.
