International Immunopharmacology,
Journal Year:
2024,
Volume and Issue:
143, P. 113468 - 113468
Published: Oct. 28, 2024
Diacetylmorphine
(DA)
is
widely
implicated
in
neuronal
injury;
however,
the
underlying
mechanisms
remain
unclear.
We
investigated
role
of
iron
metamorphosis
DA-induced
neurotoxicity
using
Sprague-Dawley
rats
and
PC12
SH-SY5Y
cells.
Tandem
mass
tag
proteomics
analysis
showed
that
upregulation
protein
kinase
C
delta
(PKCδ)
metabolism-related
transferrin
receptor
(TFRC)
significantly
enriched
metabolism
pathway.
Subsequent
experiments
DA
exposure
upregulated
PKCδ
cells,
which
increased
nuclear
translocation
specificity
1
(SP1),
intracellular
free
lipid
peroxide
levels.
In
addition,
silencing
improved
behaviour
restored
expression
level
glutathione
peroxidase
4
(GPX4).
activated
mitochondrial
autophagy
leading
to
a
decrease
membrane
potential,
accumulation
reactive
oxygen
species
(ROS),
elevation
LC3
(which
plays
key
autophagy),
p62
expression.
Following
inhibition
autophagy,
potential
ROS
were
restored,
as
was
voltage-dependent
anion
channel
(VDAC1)
GPX4.
conclusion,
present
study
suggests
regulates
SP1,
further
exacerbating
ferroptosis.
Therefore,
or
ferroptosis
may
be
therapeutic
target
ameliorate
following
exposure.
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(4), P. 395 - 395
Published: March 26, 2024
Central
neurological
disorders
are
significant
contributors
to
morbidity,
mortality,
and
long-term
disability
globally
in
modern
society.
These
encompass
neurodegenerative
diseases,
ischemic
brain
traumatic
injury,
epilepsy,
depression,
more.
The
involved
pathogenesis
is
notably
intricate
diverse.
Ferroptosis
neuroinflammation
play
pivotal
roles
elucidating
the
causes
of
cognitive
impairment
stemming
from
these
diseases.
Given
concurrent
occurrence
ferroptosis
due
metabolic
shifts
such
as
iron
ROS,
well
their
critical
central
nervous
disorders,
investigation
into
co-regulatory
mechanism
has
emerged
a
prominent
area
research.
This
paper
delves
mechanisms
along
with
interrelationship.
It
specifically
emphasizes
core
molecules
within
shared
pathways
governing
neuroinflammation,
including
SIRT1,
Nrf2,
NF-κB,
Cox-2,
iNOS/NO·,
how
different
immune
cells
structures
contribute
dysfunction
through
mechanisms.
Researchers’
findings
suggest
that
mutually
promote
each
other
may
represent
key
factors
progression
disorders.
A
deeper
comprehension
common
pathway
between
cellular
holds
promise
for
improving
symptoms
prognosis
related
Nature Communications,
Journal Year:
2025,
Volume and Issue:
16(1)
Published: Jan. 2, 2025
Alzheimer's
disease
is
characterized
by
progressive
amyloid
deposition
and
cognitive
decline,
yet
the
pathological
mechanisms
treatments
remain
elusive.
Here
we
report
therapeutic
potential
of
low-intensity
40
hertz
blue
light
exposure
in
a
5xFAD
mouse
model
disease.
Our
findings
reveal
that
treatment
prevents
memory
decline
4-month-old
mice
motivation
loss
14-month-old
mice,
accompanied
restoration
glial
water
channel
aquaporin-4
polarity,
improved
brain
drainage
efficiency,
reduction
hippocampal
lipid
accumulation.
We
further
demonstrate
beneficial
effects
are
mediated
through
activation
vLGN/IGL-Re
visual
circuit.
Notably,
concomitant
use
anti-Aβ
antibody
with
demonstrates
soluble
Aβ
clearance
performance
mice.
These
offer
functional
evidence
on
Aβ-related
pathologies
suggest
its
as
supplementary
strategy
to
augment
efficacy
antibody-based
therapy.
Treatments
for
(AD)
limited.
Here,
authors
show
activates
circuit
boost
glymphatic
drainage,
enhances
memory,
motivation,
therapy
AD.
Molecular Cancer,
Journal Year:
2024,
Volume and Issue:
23(1)
Published: Aug. 27, 2024
Abstract
The
development
of
drug
resistance
remains
a
major
challenge
in
cancer
treatment.
Ferroptosis,
unique
type
regulated
cell
death,
plays
pivotal
role
inhibiting
tumour
growth,
presenting
new
opportunities
treating
chemotherapeutic
resistance.
Accumulating
studies
indicate
that
epigenetic
modifications
by
non-coding
RNAs
(ncRNA)
can
determine
vulnerability
to
ferroptosis.
In
this
review,
we
first
summarize
the
growth/development.
Then,
core
molecular
mechanisms
ferroptosis,
its
upstream
regulation,
and
downstream
effects
on
Finally,
review
recent
advances
understanding
how
ncRNAs
regulate
ferroptosis
from
such
modulate
This
aims
enhance
general
ncRNA-mediated
regulatory
which
highlighting
ncRNA-ferroptosis
axis
as
key
druggable
target
overcoming
Frontiers in Cell and Developmental Biology,
Journal Year:
2025,
Volume and Issue:
13
Published: March 21, 2025
Ferroptosis,
a
non-apoptotic,
iron-dependent
form
of
regulated
cell
death,
is
closely
related
to
the
pathogenesis
neurodegenerative
diseases.
Stem
cells
and
their
derivatives
exhibit
remarkable
potential
in
modulating
ferroptosis,
offering
promising
therapeutic
intervention
for
In
this
review,
we
systematically
explore
neurological
aging
its
association
with
cognitive
impairment
diseases,
focus
on
molecular
mechanisms
ferroptosis
diseases
strategies
stem
Frontiers in Molecular Neuroscience,
Journal Year:
2025,
Volume and Issue:
18
Published: May 1, 2025
Maintaining
proteostasis
is
critical
for
neuronal
health,
with
its
disruption
underpinning
the
progression
of
neurodegenerative
diseases
such
as
Alzheimer’s,
Parkinson’s,
and
Huntington’s
diseases.
Nuclear
Factor
Erythroid
2-Related
1
(NFE2L1)
has
emerged
a
key
regulator
proteostasis,
integrating
proteasome
function,
autophagy,
ferroptosis
to
counteract
oxidative
stress
protein
misfolding.
This
review
synthesizes
current
knowledge
on
role
NFE2L1
in
maintaining
homeostasis,
focusing
mechanisms
mitigating
proteotoxic
supporting
cellular
offering
protection
against
neurodegeneration.
Furthermore,
we
discuss
pathological
implications
dysfunction
explore
potential
therapeutic
target.
By
highlighting
gaps
understanding
presenting
future
research
directions,
this
aims
elucidate
NFE2L1’s
advancing
treatment
strategies
Molecular Medicine,
Journal Year:
2025,
Volume and Issue:
31(1)
Published: April 26, 2025
Abstract
The
irreversible
degeneration
of
dopamine
neurons
induced
by
α-synuclein
(α-syn)
aggregation
in
the
substantia
nigra
is
central
pathological
feature
Parkinson's
disease
(PD).
Neuroimaging
and
autopsy
studies
consistently
confirm
significant
iron
accumulation
brain
PD
patients,
suggesting
a
critical
role
for
progression.
Current
research
has
established
that
overload
induces
ferroptosis
dopaminergic
neurons,
evidence
indicates
impact
on
pathology
extends
beyond
ferroptosis.
Iron
also
plays
regulatory
modulating
α-syn,
affecting
its
aggregation,
spatial
conformation,
post-translational
modifications,
mRNA
stability.
Iron-induced
α-syn
can
contribute
to
neurodegeneration
through
additional
mechanisms,
potentially
creating
feedback
loop
which
further
enhances
accumulation,
thus
perpetuating
vicious
cycle
neurotoxicity.
Given
α-syn’s
intrinsically
disordered
structure,
targeting
metabolism
presents
promising
therapeutic
strategy
PD.
Therefore,
development
chelators,
alone
or
combination
with
other
drugs,
may
offer
beneficial
approach
alleviating
symptoms
slowing
