ABSTRACT
Background
Spinal
cord
injury
(SCI)
is
a
complex
central
nervous
system
disorder
characterized
by
multifaceted
pathological
processes,
including
inflammation,
oxidative
stress,
programmed
cell
death,
autophagy,
and
mitochondrial
dysfunction.
Sirtuin
1
(Sirt1),
critical
NAD
+
‐dependent
deacetylase,
has
emerged
as
promising
therapeutic
target
for
SCI
repair
due
to
its
potential
protect
neurons,
regulate
glial
vascular
cells,
optimize
the
microenvironment.
However,
regulatory
roles
of
Sirt1
in
are
challenging,
effects
vary
depending
on
activation
timing,
expression
levels,
types.
Methods
A
systematic
literature
review
was
conducted
using
PubMed,
Scopus,
Web
Science
identify
studies
investigating
SCI.
Relevant
publications
were
analyzed
synthesize
current
evidence
Sirt1's
mechanisms,
effects,
challenges
repair.
Results
exerts
broad
across
diverse
processes
types
post‐SCI.
It
promotes
neuronal
survival
axonal
regeneration,
modulates
astrocytes
microglia
resolve
supports
oligodendrocyte‐mediated
myelination,
enhances
endothelial
function.
Proper
may
mitigate
secondary
injury,
whereas
excessive
or
prolonged
could
impair
inflammatory
resolution
disrupt
cellular
homeostasis.
This
highlights
therapies,
but
include
optimizing
spatiotemporal
addressing
dual
different
Conclusion
Targeting
represents
viable
strategy
repair,
given
regulation
neuroprotection,
immunomodulation,
tissue
remodeling.
translating
these
findings
into
therapies
requires
resolving
issues
such
type‐specific
delivery,
precise
dosage
control.
provides
theoretical
foundation
practical
insights
advancing
Sirt1‐based
treatments
Journal of Nanobiotechnology,
Journal Year:
2025,
Volume and Issue:
23(1)
Published: Feb. 19, 2025
Intracerebral
haemorrhage
(ICH)
is
a
devastating
neurological
disorder
with
high
morbidity
and
mortality
rates,
largely
owing
to
the
lack
of
effective
therapeutic
strategies.
Growing
evidence
has
underscored
pivotal
role
ferroptosis
in
intracerebral
haemorrhage,
its
contribution
neuronal
death
exacerbation
brain
injury,
thus
establishing
it
as
crucial
target
for
intervention.
In
recent
years,
polyoxometalate
nanoclusters
(NCs)
have
been
applied
various
neurodegenerative
diseases,
demonstrating
neuroprotective
effects.
However,
their
impact
on
iron
content
function
following
ICH
yet
be
reported.
Here,
we
explored
potential
tungsten-based
(W-POM)
NCs
inhibitors
targeting
metabolic
pathway
mediated
by
S100A8/A9
treatment
ICH.
We
successfully
synthesized
ultra-small
reduced
W-POM
that
can
rapidly
cross
blood-brain
barrier
are
cleared
through
kidney.
vitro
experiments
demonstrated
exhibit
significant
stable
ROS
scavenging
activity
while
effectively
alleviating
overload
associated
damage.
vivo,
restored
metabolism
homeostasis,
suppressed
neuroinflammation
oxidative
stress,
ultimately
severe
damage
motor
deficits
mice.
Proteomic
combined
bioinformatic
analyses
identified
two
core
genes,
S100A8
S100A9,
most
intervention
Further
confirmed
act
modulating
toll-like
receptor
4/hepcidin/ferroportin
signaling
pathway,
thereby
regulating
reducing
secondary
injury.
This
study
pioneers
application
polyoxometalates
offering
novel
promising
approach
management
ferroptosis-related
injuries.
