Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: Aug. 29, 2024
Traumatic
spinal
cord
injury
(tSCI)
is
a
severe
to
the
central
nervous
system
that
categorized
into
primary
and
secondary
injuries.
Among
them,
local
microenvironmental
imbalance
in
caused
by
includes
accumulation
of
cytokines
chemokines,
reduced
angiogenesis,
dysregulation
cellular
energy
metabolism,
dysfunction
immune
cells
at
site
injury,
which
severely
impedes
neurological
recovery
from
(SCI).
In
recent
years,
single-cell
techniques
have
revealed
heterogeneity
multiple
genomic,
transcriptomic,
proteomic,
metabolomic
levels
after
tSCI,
further
deepening
our
understanding
mechanisms
underlying
tSCI.
However,
spatial
information
about
tSCI
microenvironment,
such
as
cell
location
cell-cell
interactions,
lost
these
approaches.
The
application
multi-omics
technology
can
solve
this
problem
combining
data
obtained
immunohistochemistry
multiparametric
analysis
reveal
changes
microenvironment
different
times
SCI.
review,
we
systematically
review
progress
study
SCI,
including
discuss
potential
future
therapeutic
strategies.
ABSTRACT
Background
Vascular
dementia
(VaD)
includes
a
group
of
brain
disorders
that
are
characterized
by
cerebrovascular
pathology.Neuroinflammation,
disruption
the
blood–brain
barrier
(BBB)
permeability,
white
matter
lesions,
and
neuronal
loss
all
significant
pathological
manifestations
VaD
play
key
role
in
disease
progression.
Necroptosis,
also
known
asprogrammed
necrosis,
is
mode
programmed
cell
death
distinct
from
apoptosis
closely
associated
with
ischemic
injury
neurodegenerative
diseases.
Recent
studies
have
shown
necroptosis
exacerbates
BBB
destruction,
activates
neuroinflammation,
promotes
loss,
severely
affects
prognosis.
Results
Conclusions
In
this
review,
we
outline
roles
its
molecular
mechanisms
process
VaD,
particular
focus
on
modulating
neuroinflammation
exacerbating
permeability
elaborate
regulatory
centrally
involved
cells
mediated
tumor
necrosis
factor‐α
VaD.
We
analyze
possibility
specific
strategy
targeting
would
help
inhibit
destruction
With
necroptosis,
study
delved
into
impact
changes
prognosis
to
provide
new
treatment
ideas.
Communications Biology,
Journal Year:
2025,
Volume and Issue:
8(1)
Published: Feb. 7, 2025
Age-related
long-term
disability
is
attracting
increasing
attention
due
to
the
growing
ageing
population
worldwide.
However,
current
understanding
of
senescent
spinal
cord
remains
insufficient.
Bulk
RNA
sequencing
reveals
that
526
genes
are
upregulated
and
300
downregulated
in
cords.
Pathway
enrichment
analysis
differentially
expressed
shows
senescence
cords
related
phagosome
function,
neuroinflammation,
ferroptosis,
necroptosis.
Prediction
upstream
transcription
factors
interactome
identify
Spi1
as
a
factor
potentially
plays
core
role
Spatial
transcriptomics
illustrates
spatial
distribution
transcriptomic
landscape
both
young
identifies
distinct
neuronal
glial
subtypes.
The
ferroptosis-associated
gene
Fth1
aged
Flow
cytometry
increased
accumulation
free
Fe2+
ROS
mixed
cells;
however,
CCK-8
assays
reveal
these
cells
resistant
ferroptosis.
SiRNA
lentivirus
experiments
indicate
overexpression
normal
reduces
their
sensitivity
whereas
knockdown
increases
In
summary,
bulk
elucidate
transcriptional
characteristics
versus
cords,
thus
highlighting
mediating
ferroptosis
resistance
cells.
Multiomics
sheds
light
on
expression
signature
during
process-resistance
via
upregulation
Fth1.
Cell Reports,
Journal Year:
2025,
Volume and Issue:
44(2), P. 115298 - 115298
Published: Feb. 1, 2025
Highlights•RGCs
demonstrate
similar
gene
expression
changes
during
EAE
and
aging•RGCs
exhibit
DNA
damage,
chromatin
mark
changes,
nuclear
lamina
dystrophy
in
EAE•Patients
with
MS
damage
senescence-associated
neurons•AAV2-OSK
limits
RGC
death
preserves
visual
acuity
EAESummaryIn
multiple
sclerosis
(MS),
inflammation
of
the
central
nervous
system
results
demyelination,
neuroaxonal
injury,
cell
death.
However,
molecular
signals
responsible
for
injury
neurons
are
not
fully
characterized.
Here,
we
profile
transcriptome
retinal
ganglion
cells
(RGCs)
experimental
autoimmune
encephalomyelitis
(EAE)
mice.
Pathway
analysis
identifies
a
transcriptional
signature
reminiscent
aged
RGCs
some
senescent
features,
comparable
present
from
patients
MS.
This
is
supported
by
immunostaining
demonstrating
alterations
to
envelope,
modifications
marks,
accumulation
damage.
Transduction
an
Oct4-Sox2-Klf4
adeno-associated
virus
(AAV)
rejuvenate
enhances
survival
improves
acuity.
Collectively,
these
data
reveal
aging-like
phenotype
under
pathological
neuroinflammation
support
possibility
that
rejuvenation
therapies
or
senotherapeutic
agents
could
offer
direct
avenue
neuroprotection
neuroimmune
disorders.Graphical
abstract
