Neural Regeneration Research,
Journal Year:
2024,
Volume and Issue:
20(8), P. 2199 - 2217
Published: July 29, 2024
Reperfusion
following
cerebral
ischemia
causes
both
structural
and
functional
damage
to
brain
tissue
could
aggravate
a
patient’s
condition;
this
phenomenon
is
known
as
ischemia-reperfusion
injury.
Current
studies
have
elucidated
the
neuroprotective
role
of
sirtuin
protein
family
(Sirtuins)
in
modulating
However,
potential
utilizing
it
novel
intervention
target
influence
prognosis
injury
requires
additional
exploration.
In
review,
origin
research
progress
Sirtuins
are
summarized,
suggesting
involvement
diverse
mechanisms
that
affect
injury,
including
inflammation,
oxidative
stress,
blood–brain
barrier
damage,
apoptosis,
pyroptosis,
autophagy.
The
therapeutic
avenues
related
may
improve
were
also
investigated
by
expression
affecting
representative
pathways,
such
nuclear
factor-kappa
B
signaling,
stress
mediated
adenosine
monophosphate-activated
kinase,
forkhead
box
O.
This
review
summarizes
endogenous
substances,
RNA
hormones,
drugs,
dietary
supplements,
emerging
therapies
regulate
expression.
reveals
regulating
mitigates
when
combined
with
other
risk
factors.
While
show
promise
for
treatment
most
recent
based
on
rodent
models
circadian
rhythms
distinct
from
those
humans,
potentially
influencing
efficacy
Sirtuins-targeting
drug
therapies.
Overall,
provides
new
insights
into
pathology
European Journal of Pharmaceutical Sciences,
Journal Year:
2025,
Volume and Issue:
unknown, P. 107099 - 107099
Published: April 1, 2025
Ischemia
is
a
major
contributor
to
acute
kidney
injury
(AKI),
for
which
current
treatment
options
remain
limited.
One
NAD+-dependent
deacetylase
that
can
preserve
renal
cells
SIRT1.
To
date,
no
research
has
directly
explored
the
effects
of
E1231,
SIRT1
activator,
in
context
ischemia-reperfusion
(IR)
injury.
Enhancing
NAD+
levels
essential
sustaining
activity.
Hence,
combined
use
E1231
and
SR647,
precursor,
could
potentially
amplify
protective
by
supporting
prolonged
activation.
This
study
first
investigate
therapeutic
potential
combining
SR647
mitigating
unilateral
IR
Rats
treated
with
E1231/SR647
effectively
demonstrated
reduced
tubular
damage,
inflammation,
necrosis.
These
improvements
correlated
kidney-to-body
weight
ratio
increased
urine
output
flow
rate.
Additionally,
rats
reductions
serum
creatinine,
BUN,
UAER,
cystatin
C,
as
well
urinary
NGAL
both
KIM-1
levels.
On
other
hand,
elevations
creatinine
CL
were
recorded.
alone
provided
moderate
functional
recovery,
was
negated
when
co-administered
inhibitor.
upregulated
activity,
subsequently
enhancing
FOXO3
It
also
boosted
Nrf2
upregulating
antioxidant
protein
expression
HO-1
NQO1.
Furthermore,
inflammatory
response
inhibiting
NFκB
In
conclusion,
promising
therapy
may
protect
function
during
ischemic
events
through
modulation
SIRT1/FOXO3
control
over
pathways.
Cell Death Discovery,
Journal Year:
2025,
Volume and Issue:
11(1)
Published: April 21, 2025
Abstract
Nuclear
factor
erythroid
2-related
2
(NRF2)
is
a
key
transcription
involved
in
regulating
cellular
antioxidant
defense
and
detoxification
mechanisms.
It
mitigates
oxidative
stress
xenobiotic-induced
damage
by
inducing
the
expression
of
cytoprotective
enzymes,
including
HO-1
NQO1.
NRF2
also
modulates
inflammatory
responses
inhibiting
pro-inflammatory
genes
mediates
cell
death
pathways,
apoptosis
ferroptosis.
Targeting
offers
potential
therapeutic
avenues
for
treating
various
diseases.
regulated
through
two
principal
mechanisms:
post-translational
modifications
(PTMs)
epigenetic
alterations.
PTMs,
phosphorylation,
ubiquitination,
acetylation,
play
pivotal
role
modulating
NRF2’s
stability,
activity,
subcellular
localization,
thereby
precisely
controlling
its
function
response.
For
instance,
ubiquitination
can
lead
to
degradation
reduced
while
deubiquitination
enhances
stability
function.
Epigenetic
modifications,
such
as
DNA
methylation,
histone
interactions
with
non-coding
RNAs
(e.g.,
MALAT1,
PVT1,
MIR4435-2HG,
TUG1),
are
essential
chromatin
architecture
gene
accessibility.
This
paper
systematically
summarizes
molecular
mechanisms
which
PTMs
alterations
regulate
NRF2,
elucidates
critical
disease.
By
analyzing
impact
well
RNA
on
expression,
study
reveals
complex
protection
network
mediated
NRF2.
Furthermore,
explores
how
these
regulatory
affect
roles
stress,
inflammation,
death,
identifying
novel
targets
strategies.
provides
new
insights
into
treatment
NRF2-related
diseases,
cancer,
neurodegenerative
disorders,
metabolic
syndrome.
research
deepens
our
understanding
homeostasis
lays
foundation
development
NRF2-targeted
therapies.
