Research Square (Research Square),
Год журнала:
2023,
Номер
unknown
Опубликована: Ноя. 21, 2023
Abstract
Background
In
the
context
of
development
Intervertebral
Disc
Degeneration
(IDD),
inflammatory
mediators
play
a
pivotal
role.
Nevertheless,
due
to
influence
microenvironment,
causal
relationship
between
specific
and
IDD
remains
uncertain.
Methods
We
utilized
genetic
data
concerning
systemic
circulating
regulators
obtained
from
Genome-Wide
Association
Study
(GWAS)
analyzing
41
serum
cytokines
in
cohort
8,293
individuals
Finland.
The
for
was
derived
most
recent
summary
statistics
conducted
within
FinnGen
consortium,
encompassing
37,636
cases
270,964
controls.
Our
analysis
employed
bidirectional
two-sample
Mendelian
randomization
(MR)
techniques,
which
included
several
MR
methods
such
as
Egger,
weighted
median,
inverse
variance
(IVW),
mode,
simple
mode.
Additionally,
MR-PRESSO
method
identify
horizontal
pleiotropy,
heterogeneity
quantified
using
Cochran
Q
statistic,
Egger
intercept
performed
assess
pleiotropy.
Results
established
relationships
three
factors
IDD.
Elevated
levels
MIP-1β
[OR
=
0.956,
95%
CI:
-0.08
-0.006;
P
0.02]
IFN-G
0.915,
-0.16
-0.02;
0.01]
expression
were
associated
with
reduced
risk
Conversely,
susceptibility
linked
decrease
IL13
0.967,
-0.063
-0.004;
0.03].
Conclusion
this
study,
we
have
identified
that
exhibit
onset
progression
IDD,
supported
by
predictions.
ABSTRACT
Background
Resistin
may
connect
obesity
and
intervertebral
disc
(IVD)
degeneration
(IDD)
is
linked
with
chronic
inflammation.
Furthermore,
human
IDD
characterized
by
high
expression
of
interleukin‐20
(IL‐20).
The
response
nucleus
pulposus
(NP)
cells
to
tensile
forces
depends
on
both
the
duration
magnitude
force
applied.
Nonetheless,
interactions
among
resistin,
IL‐20,
in
regulating
function
IVD
NP
remain
yet
be
fully
understood.
Nuclear
factor
erythroid
2‐related
2
(NRF2)
has
been
identified
as
a
pleiotropic
protein
that
enhances
cellular
resistance
stress
stimuli
inflammatory
challenges.
role
NRF2
not
well
defined,
whether
influences
levels
known.
Aims
This
study
investigated
subjected
low‐frequency
cyclic
stretch
stimulation,
underlying
mechanisms
involved.
Materials
Methods
Human
were
cultured
chambers,
serum‐starved
for
12
h,
then
5%
strain
at
0.1
Hz
bioreactor.
Control
chambers
had
no
stretching.
Cells
lysed
analysis
post‐loading.
Results
stimulation
induced
IL‐20
dose‐
time‐dependent
manner.
activation
p38
mitogen‐activated
kinase,
Akt
signaling
pathways,
production
toll‐like
receptor
4,
are
necessary
render
resistin
cause
release
IL‐20.
In
cells,
transcription
enzyme‐linked
immunosorbent
assays
revealed
led
an
increase
nuclear
(NF)‐κB‐DNA
binding
activities.
Exposure
inhibited
this
resistin‐induced
NF‐κB
expression.
Discussion
These
findings
elucidate
molecular
through
which
induces
also
demonstrate
can
protect
against
induction.
Molecular Medicine,
Год журнала:
2024,
Номер
30(1)
Опубликована: Авг. 9, 2024
Lipid
metabolism
disorders
are
associated
with
degeneration
of
multiple
tissues
and
organs,
but
the
mechanism
crosstalk
between
lipid
disorder
intervertebral
disc
(IDD)
has
not
been
fully
elucidated.
In
this
study
we
aim
to
investigate
regulatory
abnormal
signal
on
endplate
chondrocyte
(EPC)
senescence
calcification.
Frontiers in Nutrition,
Год журнала:
2025,
Номер
12
Опубликована: Март 10, 2025
Lipid
metabolism
encompasses
the
processes
of
digestion,
absorption,
synthesis,
and
degradation
fats
within
biological
systems,
playing
a
crucial
role
in
sustaining
normal
physiological
functions.
Disorders
lipid
metabolism,
characterized
by
abnormal
blood
levels
dysregulated
fatty
acid
have
emerged
as
significant
contributors
to
intervertebral
disk
degeneration
(IDD).
The
pathogenesis
IDD
is
multifaceted,
encompassing
genetic
predispositions,
nutritional
metabolic
factors,
mechanical
stressors,
trauma,
inflammatory
responses,
which
collectively
facilitate
progression
IDD.
Although
precise
mechanisms
underlying
remain
incompletely
elucidated,
there
substantial
consensus
regarding
close
association
between
disorders
its
development.
Intervertebral
disks
are
essential
for
maintaining
spinal
alignment.
Their
primary
functions
encompass
shock
preservation
curvature,
facilitation
movement,
provision
stability.
elasticity
thickness
these
effectively
absorb
daily
impacts,
safeguard
spine,
uphold
natural
curvature
flexibility,
while
also
creating
space
nerve
roots
prevent
compression
ensure
transmission
signals.
Research
indicates
that
such
disturbances
may
compromise
functionality
cartilaginous
endplates
(CEP)
nucleus
pulposus
(NP),
thereby
facilitating
IDD’s
onset
progression.
CEP
integral
internal
material
exchange
absorption
mitigating
NP
herniation
under
load
conditions.
As
central
component
disks,
height
providing
shock-absorbing
capabilities;
thus,
damage
critical
structures
accelerates
Furthermore,
contribute
through
including
activation
endoplasmic
reticulum
stress
pathways,
enhancement
oxidative
levels,
induction
cellular
pyroptosis
alongside
inhibition
autophagy
processes—coupled
with
promotion
inflammation-induced
fibrosis
fibroblast
proliferation
leading
calcification
disks.
This
review
delineates
intricate
interplay
IDD;
it
anticipated
advancing
our
understanding
this
will
pave
way
more
effective
preventive
measures
therapeutic
strategies
against
future
research.
Experimental Gerontology,
Год журнала:
2024,
Номер
188, С. 112380 - 112380
Опубликована: Фев. 22, 2024
Intervertebral
disc
degeneration
(IVDD)
constitutes
a
crucial
pathological
foundation
for
spinal
degenerative
diseases
(SDD)
and
stands
as
primary
contributor
to
both
low
back
pain
(LBP)
disability.
The
progression
of
IVDD
is
linked
structural
functional
alterations
in
tissues,
where
an
imbalance
the
inflammatory
microenvironment
can
induce
extracellular
matrix
(ECM)
degradation,
senescence,
apoptosis.
This
key
pathomechanism
disease's
development,
gaining
considerable
attention
recent
years.
study
aims
conduct
bibliometric
analysis
publications
pertaining
mechanisms
quantitatively
assess
current
research
hotspots
directions.
