Drug Development Research,
Journal Year:
2024,
Volume and Issue:
85(8)
Published: Dec. 1, 2024
ABSTRACT
Cerebral
ischemia/reperfusion
injury
is
one
of
the
main
causes
neuronal
damage.
Neuron
ferroptosis
and
microglia
polarization
are
considered
as
critical
processes
during
cerebral
ischemia/reperfusion.
Adipocyte
enhancer‐binding
protein
1
(AEBP1)
usually
acts
a
transcriptional
repressor
which
involved
in
various
diseases.
However,
it
still
remains
unknown
whether
AEBP1
could
have
important
roles
regulating
neuron
injury.
The
oxygen‐glucose
deprivation
reperfusion
(OGD/R)‐treated
cells
middle
artery
occlusion
(MCAO)‐treated
mice
were
used
vitro
vivo
models.
differentially
expressed
factors
analyzed
according
to
GEO
datasets.
Relative
mRNA
expression
levels
detected
by
qRT‐PCR
western
blot
analysis.
Cell
viability
was
measured
CCK‐8
assay.
ROS,
GSH
iron
contents
using
specifical
assay
kits.
CD26
CD206
immunofluorescence
Inflammatory
cytokines
ELISA.
association
between
PRKCA
assessed
luciferase
reporter
ChIP
analyses.
damage
TTC
staining
neurological
deficit
score.
Transcription
factor
increased
OGD/R‐treated
HT22
BV2
cells.
silencing
attenuated
OGD/R‐induced
cell
through
increasing
viability,
GPX4
levels,
decreasing
ACSL4
levels.
knockdown
promoted
M2
CD206‐positive
Arg‐1
level,
reducing
iNOS,
TNF‐α,
IL‐1β
IL‐6
transcriptionally
repressed
expression,
further
regulated
PI3K/Akt
signaling
activation.
Inhibition
or
reversed
effects
on
polarization.
downregulation
infarct
size
scores
MCAO‐treated
mice.
mitigated
activating
signaling,
indicating
potentially
protective
action
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(20), P. 10926 - 10926
Published: Oct. 11, 2024
Circadian
rhythms,
the
internal
timekeeping
systems
governing
physiological
processes,
significantly
influence
skin
health,
particularly
in
response
to
ultraviolet
radiation
(UVR).
Disruptions
circadian
rhythms
can
exacerbate
UVR-induced
damage
and
increase
risk
of
aging
cancer.
This
review
explores
how
affect
various
aspects
physiology
pathology,
with
a
special
focus
on
DNA
repair.
regulation
ensures
optimal
repair
following
damage,
reducing
mutation
accumulation,
enhancing
genomic
stability.
The
control
over
cell
proliferation
apoptosis
further
contributes
regeneration
UVR.
Oxidative
stress
management
is
another
critical
area
where
exert
influence.
Key
genes
like
brain
muscle
ARNT-like
1
(BMAL1)
locomotor
output
cycles
kaput
(CLOCK)
modulate
activity
antioxidant
enzymes
signaling
pathways
protect
cells
from
oxidative
stress.
also
inflammatory
immune
responses
by
modulating
Langerhans
other
skin.
In
summary,
form
complex
defense
network
that
manages
through
precise
repair,
proliferation,
apoptosis,
response,
stress,
hormonal
signaling.
Understanding
these
mechanisms
provides
insights
into
developing
targeted
protection
improving
cancer
prevention.
Cell Death Discovery,
Journal Year:
2024,
Volume and Issue:
10(1)
Published: Dec. 24, 2024
Abstract
TRIM14
is
an
important
member
of
the
TRIM
family
and
widely
expressed
in
a
variety
tissues.
Like
other
members
family,
also
involved
ubiquitination
modifications.
was
initially
reported
as
interferon-stimulated
gene
(ISG).
In
recent
years,
many
studies
have
focused
on
regulatory
role
signaling
pathways
such
PI3K/Akt,
NF-κB,
cGAS/STING
revealed
its
mechanism
action
pathophysiological
processes,
regulation
has
attracted
interest
researchers
new
direction
for
treatment
various
diseases.
However,
there
are
no
reviews
this
paper,
we
will
describe
structure
TRIM14,
review
cancer,
cardiovascular
disease,
cervical
spondylosis,
inflammation
antiviral
immunity,
provide
outlook
future
research
directions.
Journal of Cerebral Blood Flow & Metabolism,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Oct. 25, 2024
The
increasing
prevalence
of
pathological
cerebrovascular
conditions,
including
stroke,
hypertensive
encephalopathy,
and
chronic
disorders,
underscores
the
importance
anesthetic
considerations
for
affected
patients.
Preserving
cerebral
oxygenation
blood
flow
during
anesthesia
is
paramount
to
prevent
neurological
deterioration.
Furthermore,
protecting
vulnerable
neurons
from
damage
crucial
optimal
outcomes.
Recent
research
suggests
that
agents
may
provide
a
potentially
therapeutic
approach
managing
conditions.
Anesthetics
target
neural
mechanisms
underlying
dysfunction,
thereby
modulating
neuroinflammation,
against
ischemic
injury,
improving
hemodynamics.
However,
strategies
regarding
mechanisms,
dosage,
indications
remain
uncertain.
This
review
aims
clarify
physiological
effects,
action,
reported
neuroprotective
benefits
anesthetics
in
patients
with
various
Investigating
effects
disease
holds
promise
developing
novel
strategies.
Drug Development Research,
Journal Year:
2024,
Volume and Issue:
85(8)
Published: Dec. 1, 2024
ABSTRACT
Cerebral
ischemia/reperfusion
injury
is
one
of
the
main
causes
neuronal
damage.
Neuron
ferroptosis
and
microglia
polarization
are
considered
as
critical
processes
during
cerebral
ischemia/reperfusion.
Adipocyte
enhancer‐binding
protein
1
(AEBP1)
usually
acts
a
transcriptional
repressor
which
involved
in
various
diseases.
However,
it
still
remains
unknown
whether
AEBP1
could
have
important
roles
regulating
neuron
injury.
The
oxygen‐glucose
deprivation
reperfusion
(OGD/R)‐treated
cells
middle
artery
occlusion
(MCAO)‐treated
mice
were
used
vitro
vivo
models.
differentially
expressed
factors
analyzed
according
to
GEO
datasets.
Relative
mRNA
expression
levels
detected
by
qRT‐PCR
western
blot
analysis.
Cell
viability
was
measured
CCK‐8
assay.
ROS,
GSH
iron
contents
using
specifical
assay
kits.
CD26
CD206
immunofluorescence
Inflammatory
cytokines
ELISA.
association
between
PRKCA
assessed
luciferase
reporter
ChIP
analyses.
damage
TTC
staining
neurological
deficit
score.
Transcription
factor
increased
OGD/R‐treated
HT22
BV2
cells.
silencing
attenuated
OGD/R‐induced
cell
through
increasing
viability,
GPX4
levels,
decreasing
ACSL4
levels.
knockdown
promoted
M2
CD206‐positive
Arg‐1
level,
reducing
iNOS,
TNF‐α,
IL‐1β
IL‐6
transcriptionally
repressed
expression,
further
regulated
PI3K/Akt
signaling
activation.
Inhibition
or
reversed
effects
on
polarization.
downregulation
infarct
size
scores
MCAO‐treated
mice.
mitigated
activating
signaling,
indicating
potentially
protective
action
