Immunity Inflammation and Disease,
Journal Year:
2024,
Volume and Issue:
12(11)
Published: Nov. 1, 2024
ABSTRACT
Background
Intervertebral
disc
degeneration
(IDD)
is
a
major
cause
for
low
back
pain.
Studies
showed
the
association
between
senescence
and
degenerative
diseases.
Cell
can
promote
occurrence
development
of
diseases
through
multiple
mechanisms
including
inflammatory
stress,
oxidative
stress
nutritional
deprivation.
The
roles
senescence‐associated
genes
(SAGs)
remains
unknown
in
IDD.
Methods
Four
differently
expressed
SAGs
were
identified
as
hub
using
“limma“
package
R.
We
then
calculated
immune
infiltration
IDD
patients,
investigated
relation
infiltration.
Enrichment
analysis
was
performed
to
explore
functions
Nomogram
LASSO
model
based
on
constructed
predict
risk
severe
(SD)
patients.
Subsequently,
single
cell
conducted
describe
expression
pattern
intervertebral
tissue.
Results
ASPH,
CCND1,
IGFBP3
SGK1
SAGs.
Further
demonstrated
that
might
mediate
by
regulating
pathways.
four
good
performance
predicting
SD.
Single
revealed
CCND1
mainly
nucleus
pulposus
cells,
while
epithelial
cells.
Eleven
candidate
drugs
targeting
SAGS
predicted
patients
Comparative
Toxicogenomics
Database
(CDT).
PCR
immunohistochemical
levels
higher
SD
than
MD
(mild
degeneration)
Conclusions
comprehensive
IDD,
which
their
Based
SAGs,
we
established
predictive
explored
potential
drugs.
These
findings
provide
new
understandings
SAG
mechanism
promising
therapeutic
strategies
ACS Nano,
Journal Year:
2024,
Volume and Issue:
18(12), P. 8885 - 8905
Published: March 11, 2024
As
intervertebral
disc
degeneration
(IVDD)
proceeds,
the
dysfunctional
mitochondria
disrupt
viability
of
nucleus
pulposus
cells,
initiating
degradation
extracellular
matrix.
To
date,
there
is
a
lack
effective
therapies
targeting
cells.
Here,
we
synthesized
polygallic
acid-manganese
(PGA-Mn)
nanoparticles
via
self-assembly
polymerization
gallic
acid
in
an
aqueous
medium
and
introduced
mitochondrial
peptide
(TP04)
onto
using
Schiff
base
linkage,
resulting
PGA-Mn-TP04
nanoparticles.
With
size
smaller
than
50
nm,
possesses
pH-buffering
capacity,
avoiding
lysosomal
confinement
selectively
accumulating
within
through
electrostatic
interactions.
The
rapid
electron
exchange
between
manganese
ions
enhances
redox
capability
PGA-Mn-TP04,
effectively
reducing
damage
caused
by
reactive
oxygen
species.
Moreover,
restores
function
facilitating
fusion
minimizing
their
fission,
thereby
sustaining
vitality
In
rat
IVDD
model,
maintained
height
tissue
hydration.
It
offers
nonoperative
treatment
approach
for
other
skeletal
muscle
diseases
from
dysfunction,
presenting
alternative
to
traditional
surgical
interventions.
Cell Biology and Toxicology,
Journal Year:
2024,
Volume and Issue:
40(1)
Published: Oct. 21, 2024
Intervertebral
disc
degeneration
(IVDD)
is
a
primary
contributor
to
low
back
pain
and
poses
considerable
burden
society.
However,
the
molecular
mechanisms
underlying
IVDD
remain
be
elucidated.
PR/SET
domain
1
(PRDM1)
regulates
cell
proliferation,
apoptosis,
inflammatory
responses
in
various
diseases.
Despite
these
regulatory
functions,
mechanism
of
action
PRDM1
remains
unexplored.
In
this
study,
we
investigated
role
progression.
The
expression
nucleus
pulposus
(NP)
tissues
NP
cells
(NPCs)
was
assessed
using
western
blotting,
immunohistochemistry,
immunofluorescence.
effects
on
progression
were
vitro
vivo.
Mechanistically,
mRNA
sequencing,
chromatin
immunoprecipitation,
dual-luciferase
reporter
assays
performed
confirm
that
triggered
CASP1
transcription.
Our
study
demonstrated
for
first
time
substantially
upregulated
degenerated
NPCs.
overexpression
promoted
NPCs
pyroptosis
by
inhibiting
mitophagy
exacerbating
progression,
whereas
silencing
exerted
opposite
effect.
Furthermore,
activated
transcription,
thereby
promoting
vitro.
Notably,
reversed
To
best
our
knowledge,
demonstrate
inhibits
repressing
which
may
promising
new
therapeutic
target
IVDD.
JOR Spine,
Journal Year:
2025,
Volume and Issue:
8(1)
Published: Jan. 20, 2025
ABSTRACT
Background
The
molecular
of
intervertebral
disc
degeneration
(IVDD)
is
still
unclear.
When
it
comes
to
treating
decoction,
traditional
Chinese
medicine
effective.
In
particular,
the
Duhuo
(Radix
Angelicae
Biseratae)
may
be
particularly
helpful.
Purpose
To
identify
nucleus
pulposus
cells
(NPCs)
subpopulations
and
immune
clarify
mechanism
IVDD
therapy,
offering
recommendations
for
diagnosis
treatment.
Methods
targets
from
Genecards
microarray
data
biological
databases.
find
key
genes
pathways
underlying
IVDD,
multiple
machine
learning
techniques
were
used.
associated
with
NPCs
as
revealed
by
single‐cell
analysis,
immunological
infiltration
was
identified
Immune
Cell
AI.
validate
which
activity
affects
network
pharmacology
docking
employed.
Results
process
linked
like
TP53,
JUN,
PTEN,
IL1B,
ERBB2,
MAPK8,
CASP9,
PTK2,
etc.
main
mechanisms
involved
in
this
are
responses,
inflammatory
factors
expression,
cellular
responses
mechanical
stimuli,
NPC
apoptosis.
AI
discovered
a
correlation
between
CD4
naïve,
B
cell,
monocyte,
NK,
macrophage
development
IVDD.
subtypes
namely
fibroNPCs,
adhesion
NPCs,
regulatory
homeostatic
hypertrophic
chondrocyte‐like
(HT‐CL
NPCs),
subject
mapping.
We
also
found
that
Osthole,
Columbianadin,
Bergapten,
principal
blood
entry
components
Dohuo,
have
role
modulating
PTGS1,
PARP1,
Conclusion
exist
HT‐CL
NPCs.
Furthermore,
variety
cell
infiltrates,
monocyte
macrophage,
significant
impact
on
advancement
Duhuo,
absorb
via
controlling
death
Journal of Proteome Research,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 8, 2025
O-linked
beta-N-acetylglucosamine
glycosylation
(O-GlcNAcylation),
a
post-translational
modification
of
proteins,
occurs
in
multiple
physiological
and
pathological
processes.
Despite
comprehensive
study
protein
modifications,
such
as
phosphorylation,
acetylation,
ubiquitination
musculoskeletal
diseases,
the
role
O-GlcNAcylation
this
field
has
been
largely
overlooked.
However,
recent
years,
several
studies
have
initially
elucidated
biological
mechanisms
through
which
regulates
development
progress
including
osteoarthritis,
osteoporosis,
osteosarcoma,
intervertebral
disc
degeneration.
This
review
aims
to
systematically
comprehensively
summarize
existing
evidence,
sketching
contours
underlying
related
signaling
pathways,
discussing
limitations
controversies,
providing
guidance
for
future
on
modifications
diseases.