Expert Opinion on Therapeutic Targets,
Journal Year:
2024,
Volume and Issue:
unknown, P. 1 - 27
Published: Dec. 23, 2024
Introduction
Ischemic
stroke
(IS),
a
major
cause
of
mortality
and
disability
worldwide,
remains
significant
healthcare
challenge
due
to
limited
therapeutic
options.
Ferroptosis,
distinct
iron-dependent
form
regulated
cell
death
characterized
by
lipid
peroxidation
oxidative
stress,
has
emerged
as
crucial
mechanism
in
IS
pathophysiology.
This
review
explores
the
role
ferroptosis
its
potential
for
driving
innovative
strategies.
Scientific Reports,
Journal Year:
2025,
Volume and Issue:
15(1)
Published: Feb. 10, 2025
Ferroptosis
pathway
activation
is
potentially
correlated
with
temporal
lobe
epilepsy
(TLE).
However,
the
diagnostic
significance
and
mechanism
of
ferroptosis-related
genes
(FRGs)
in
TLE
require
further
investigation.
A
comprehensive
analysis
GSE134697
dataset
from
Gene
Expression
Omnibus
(GEO)
database
using
Weighted
gene
co-expression
network
(WGCNA)
identified
3,212
differentially
expressed
(DEGs)
between
(TLE)
control
groups,
a
critical
focus
on
turquoise
module.
Through
intersection
DEGs
key
module
genes,
correlation
analyses
functional-related
(FRG),
protein-protein
interactions
(PPI),
least
absolute
shrinkage
selection
operator
(LASSO),
machine
learning
methods,
five
potential
biomarkers
ferroptosis
(CBS,
SHMT1,
RIN3,
QDPR,
PLPP4)
were
isolated.
nomogram
was
constructed
these
markers,
enrichment
revealed
their
links
to
T-cell
activation,
allograft
rejection,
glial
differentiation.
Variations
13
immune
cell
types
also
noted.
Upregulation
CBS,
PLPP4
confirmed
through
RT-qPCR
Western
blot
assays.
Additionally,
SHMT1-targeting
one
CBS-targeting
drugs
predicted
Drug-Gene
Interaction
Database
(DGIdb).
These
findings
provide
new
insights
into
pathogenesis
suggest
targets
for
future
research.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(12), P. 6716 - 6716
Published: June 18, 2024
Neuropathic
pain,
which
refers
to
pain
caused
by
a
lesion
or
disease
of
the
somatosensory
system,
represents
wide
variety
peripheral
central
disorders.
Treating
neuropathic
is
quite
demanding,
primarily
because
its
intricate
underlying
etiological
mechanisms.
The
nervous
system
relies
on
microglia
maintain
balance,
as
they
are
associated
with
serving
primary
immune
responses
in
brain
next
cell
communication.
Ferroptosis,
driven
phospholipid
peroxidation
and
regulated
iron,
vital
mechanism
death
regulation.
Neuroinflammation
can
be
triggered
ferroptosis
microglia,
contributes
release
inflammatory
cytokines.
Conversely,
neuroinflammation
induce
iron
accumulation
resulting
microglial
ferroptosis.
Accumulating
evidence
suggests
that
neuroinflammation,
characterized
glial
activation
substances,
significantly
exacerbates
development
pain.
By
inhibiting
ferroptosis,
it
may
possible
prevent
subsequently
alleviate
homopentameric
α7
subtype
neuronal
nicotinic
acetylcholine
receptor
(α7nAChR)
has
potential
suppress
activation,
transitioning
M1
an
M2
phenotype,
facilitating
anti-inflammatory
factors,
ultimately
reducing
Recent
years
have
witnessed
growing
recognition
regulatory
role
α7nAChR
could
target
for
treating
This
review
summarizes
mechanisms
related
progress
according
recent
research.
Such
exploration
will
help
elucidate
relationship
between
α7nAChR,
provide
new
insights
into
management.
Pharmaceutics,
Journal Year:
2024,
Volume and Issue:
16(8), P. 1068 - 1068
Published: Aug. 15, 2024
Neuropathic
pain,
a
chronic
condition
resulting
from
nerve
injury
or
dysfunction,
presents
significant
therapeutic
challenges
and
is
closely
associated
with
oxidative
stress
inflammation,
both
of
which
can
lead
to
mitochondrial
dysfunction.
The
nuclear
factor
erythroid
2-related
2
(Nrf2)
pathway,
critical
cellular
defense
mechanism
against
stress,
has
emerged
as
promising
target
for
neuropathic
pain
management.
Nrf2
modulators
enhance
the
expression
antioxidant
cytoprotective
genes,
thereby
reducing
damage,
impairment.
This
review
explores
antinociceptive
effects
Nrf2,
highlighting
how
pharmacological
agents
natural
compounds
may
be
used
potential
strategies
pain.
Although
preclinical
studies
demonstrate
reduction
improved
function
through
activation,
several
clinical
need
addressed.
However,
emerging
evidence
suggests
benefits
in
conditions,
such
diabetic
neuropathy
multiple
sclerosis.
Future
research
should
focus
on
further
elucidating
molecular
role
optimize
its
modulation
efficacy
maximize
utility.
Fluids and Barriers of the CNS,
Journal Year:
2024,
Volume and Issue:
21(1)
Published: Nov. 21, 2024
The
Blood-Brain
Barrier
(BBB)
is
a
complex
and
dynamic
interface
that
regulates
the
exchange
of
molecules
cells
between
blood
central
nervous
system.
It
undergoes
structural
functional
throughout
oxidative
stress
inflammation,
which
may
compromise
its
integrity
contribute
to
pathogenesis
neurodegenerative
diseases.
Maintaining
BBB
utmost
importance
in
preventing
wide
range
neurological
disorders.
NRF2
main
transcription
factor
cellular
redox
balance
inflammation-related
gene
expression.
has
also
demonstrated
potential
role
regulating
tight
junction
contributing
inhibition
ECM
remodeling,
by
reducing
expression
several
metalloprotease
family
members
involved
maintaining
function.
Overall,
we
review
current
insights
on
addressing
protection
against
effects
dysfunction,
discuss
involvement
maintenance
different
neuropathological
diseases,
as
well
as,
some
activators
have
been
used
vitro
vivo
animal
models
for
barrier
dysfunction.
Thus,
emerging
evidence
suggests
upregulation
target
genes
could
suppress
stress,
neuroinflammation,
restore
integrity,
increase
protection.
Journal of Biochemical and Molecular Toxicology,
Journal Year:
2025,
Volume and Issue:
39(2)
Published: Feb. 1, 2025
Postoperative
cognitive
dysfunction
(POCD)
is
a
common
neurological
complication
after
surgery
and
general
anesthesia,
the
incidence
increases
with
age.
Will
have
negative
impact
on
patients,
family
society.
At
present,
neuroinflammation
oxidative
stress
are
main
recognized
mechanisms.
Glutathione
(GSH)
powerful
reducing
agent
may
be
related
to
POCD.
Using
medical
search
engines
such
as
PubMed,
Web
of
Science,
we
analyzed
articles
topics
as:
POCD,
GSH,
microglia,
astrocyte,
oligodendrocyte,
ferroptosis,
BDNF,
Neuroinflammation,
stress.
The
above
searched
in
databases
using
Boolean
operations.
We
included
original
articles,
reviews
other
article
types
books.
According
reviewed
literature,
GSH
treatment
for
Specific
targeted
therapies
POCD
still
sparse,
therefore,
implementation
preventive
strategies
appears
remain
optimal
attitude.
Further
research
needed
better
understanding
Frontiers in Neuroscience,
Journal Year:
2025,
Volume and Issue:
19
Published: Feb. 25, 2025
Cognitive
dysfunction
after
traumatic
brain
injury
(TBI)
significantly
reduces
quality
of
life
and
imposes
a
heavy
burden
on
society.
A
detailed
examination
research
trends
cognitive
following
TBI
has
not
yet
been
conducted.
This
study
aimed
to
examine
the
bibliometric
analysis
over
past
20
years.
Literature
was
retrieved
from
Web
Science
Core
Collection
(WoSCC)
Citation
Index
Expanded
(SCI-E)
2004
2023.
The
type
literature
language
were
refined.
total
1,902
articles
used
for
analysis,
including
1,543
(81.1%)
original
359
(18.9%)
review
articles.
Data
June
5,
2024.
publication
volume
increasing
year
by
year,
with
published
in
537
journals.
Journal
Neurotrauma,
130
articles,
most
productive
influential
journal.
University
California
System
led
number
published.
There
9,002
authors
62
countries/regions.
USA
China
top-ranked
countries
article
count.
Pandharipande
PP
authored
highly
cited
article.
Pick
CG,
as
author
highest
h-index.
top
three
keywords
injury,
impairment,
mild
injury.
topics
ferroptosis,
decline,
spinal
cord
prognosis.
Our
findings
provide
valuable
insights
into
highlight
emerging
future
research.
Brain and Behavior,
Journal Year:
2025,
Volume and Issue:
15(3)
Published: Feb. 28, 2025
ABSTRACT
Background
This
study
investigates
the
role
of
KEAP1‐NRF2/HO‐1
signaling
pathway
in
inducing
ferroptosis
and
contributing
to
neuronal
damage
schizophrenia.
Methods
We
retrieved
schizophrenia‐related
data
ferroptosis‐related
genes
from
RNA
microarray
dataset
GSE27383
FerrDB
database,
respectively.
Bioinformatics
identified
KEAP1
as
a
downregulated
gene,
which
was
validated
using
qRT‐PCR
Western
blot.
assessed
intracellular
Fe
2
⁺
content,
MDA
levels,
GSH,
GPX4
prefrontal
cortex
peripheral
blood
mononuclear
cells
(PBMCs)
patients
with
Cortical
interneurons
(cINs)
were
generated
human‐induced
pluripotent
stem
(hiPSCs)
schizophrenia
used
explore
alterations
during
neurodevelopment.
In
addition,
overexpression
induced
cINs
via
transfection
pcDNA
KEAP1.
The
Fe⁺
oxidative
stress
indicators,
lipid
peroxidation,
inflammatory
cytokines
measured
after
transfection.
To
investigate
molecular
mechanisms,
KI696—a
high‐affinity
probe
that
disrupts
KEAP1–NRF2
interaction—was
applied,
changes
stress,
peroxidation
(C11‐BODIPY
staining),
iron
metabolism,
pathways
evaluated.
Results
Patients
exhibited
underexpression
KEAP1,
key
regulator
ferroptosis,
along
elevated
levels
increased
concentrations,
indicating
enhanced
stress.
Reduced
activity
GSH
also
observed,
suggesting
an
susceptibility
ferroptosis.
further
this,
derived
hiPSCs
studied.
These
showed
decreased
expression.
Overexpression
led
reduction
concentrations
damage,
highlighting
KEAP1's
regulatory
treatment
KI696
significant
related
antioxidant
defenses,
inflammation.
Conclusion
Our
findings
indicate
contributes
injury
