Journal of Inflammation Research,
Journal Year:
2024,
Volume and Issue:
Volume 17, P. 8965 - 8984
Published: Nov. 1, 2024
Ferroptosis
is
an
underlying
mechanism
for
various
degenerative
diseases,
but
its
role
in
intervertebral
disc
degeneration
remains
elusive.
This
study
aims
to
explore
the
key
ferroptosis-related
genes
and
nucleus
pulposus
(NP)
annulus
fibrosus
(AF)
degeneration.
We
analyzed
gene
expression
profiles
of
NP
AF
from
Gene
Expression
Omnibus
database.
The
differentially
expressed
(FRDEGs)
degenerated
were
filtered,
followed
by
GO
KEGG
analysis.
Feature
FRDEGs
identified
LASSO
SVM-RFE
algorithms,
then
Set
Enrichment
Analysis
(GSEA)
Variation
(GSVA)
conducted.
Immune
infiltration
analysis
was
conducted
CIBERSORT
algorithm.
established
drug
networks
via
Drug-Gene
Interaction
Database
competitive
endogenous
RNA
(ceRNA)
miRanda,
miRDB,
TargetScan
levels
feature
assessed
validation
sets,
single-cell
RNA-seq,
experimental
verification.
A
total
15
18
obtained
AF,
respectively.
revealed
their
implication
oxidative
stress.
Four
(AKR1C1,
AKR1C3,
MUC1,
ENPP2)
five
(SCP2,
ABCC1,
KLF2,
IDO1,
CREB3)
GSEA
GSVA
showed
that
these
enriched
lots
biological
functions,
including
immune
response.
CREB3
negatively
correlated
with
Eosinophils
drugs
ceRNAs
targeting
MUC1
identified.
Experimental
verification
RNA-seq
downregulated
considered
novel
biomarkers
ferroptosis,
Drug
ceRNA
constructed
future
development
investigation
new
mechanisms
ferroptosis.
Journal of Translational Medicine,
Journal Year:
2024,
Volume and Issue:
22(1)
Published: Oct. 15, 2024
The
prevalence
of
age-related
degenerative
joint
diseases,
particularly
intervertebral
disc
degeneration
and
osteoarthritis,
is
increasing,
thereby
posing
significant
challenges
for
the
elderly
population.
Mitochondrial
dysfunction
a
critical
factor
in
etiology
progression
these
disorders.
Therapeutic
interventions
that
incorporate
mitochondrial
transplantation
exhibit
considerable
promise
by
increasing
numbers
improving
their
functionality.
Existing
evidence
suggests
exogenous
therapy
improves
clinical
outcomes
patients
with
diseases.
This
review
elucidates
abnormalities
associated
diseases
examines
mechanisms
intercellular
transfer
artificial
transplantation.
Furthermore,
therapeutic
strategies
are
synthesized,
concept
engineered
proposed.
Frontiers in Nutrition,
Journal Year:
2025,
Volume and Issue:
12
Published: March 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.
Mitochondria
are
vital
for
energy
production,
metabolic
regulation,
and
cellular
signaling.
Their
dysfunction
is
strongly
implicated
in
neurological,
cardiovascular,
muscular
degenerative
diseases,
where
deficits
oxidative
stress
accelerate
disease
progression.
Platelet
extracellular
vesicles
(PEVs),
once
called
"platelet
dust",
have
emerged
as
promising
agents
mitigating
mitochondrial
dysfunction.
Like
other
(EVs),
PEVs
carry
diverse
molecular
cargo
surface
markers
processes
therapeutic
efficacy.
Notably,
they
may
possibly
contain
intact
or
partially
functional
components,
making
them
tentatively
attractive
targeting
damage.
Although
direct
research
on
PEVs-mediated
rescue
remains
limited,
current
evidence
suggests
that
can
modulate
diseases
associated
with
potentially
enhance
health.
This
review
explores
the
potential
of
neurodegenerative
cardiovascular
disorders,
highlighting
their
role
restoring
By
examining
recent
advancements
research,
we
aim
to
shed
light
novel
strategies
utilizing
agents.
Our
goal
underscore
importance
further
fundamental
applied
into
PEVs-based
interventions,
innovative
tools
combating
a
wide
range
linked
JOR Spine,
Journal Year:
2025,
Volume and Issue:
8(1)
Published: March 1, 2025
ABSTRACT
Background
Intervertebral
disc
degeneration
(IDD)
is
a
major
cause
of
cervical
and
lumbar
diseases,
significantly
impacting
patients'
quality
life.
Mitochondria
cell
death
have
been
implicated
in
IDD,
but
the
key
related
genes
remain
unknown.
Methods
Differentially
expressed
(DEGs)
between
IDD
control
samples
were
identified
using
GSE70362.
Mitochondria‐related
(MRGs)
programmed
death‐related
(PCDRGs)
intersected
with
DEGs
to
find
DE‐MRGs
DE‐PCDRGs.
Weighted
gene
co‐expression
network
analysis
(WGCNA)
module
genes,
overlap
revealed
candidate
genes.
Mendelian
randomization
(MR)
was
used
determine
causally
linked
IDD.
Machine
learning
expression
validation
further
refined
which
then
build
nomogram
predict
risk.
Additionally,
set
enrichment
(GSEA),
immune
infiltration,
single‐cell
performed.
Results
A
total
515
224
yielding
31
Six
genes—BCKDHB,
BID,
TNFAIP6,
VRK1,
CAB39L,
TMTC1—showed
causal
relationship
TMTC1
as
through
machine
validation.
developed
based
on
these
GSEA
BID
enriched
N‐glycan
biosynthesis,
TNFAIP6
aminoacyl
tRNA
ribosomal
pathways.
Activated
dendritic
cells,
CD56dim
natural
killer
monocytes,
other
cells
elevated
strongly
correlating
activated
cells.
Key
at
higher
levels
degraded
samples.
Conclusion
TMTC1,
mitochondria
offering
new
insights
for
diagnosis
treatment.
Brazilian Journal of Medical and Biological Research,
Journal Year:
2025,
Volume and Issue:
58
Published: Jan. 1, 2025
Low
back
pain
(LBP)
is
a
common
type
of
that
causes
disability
and
impairs
cognitive
function.
With
over
80%
adults
estimated
to
experience
LBP
during
their
lifetime,
this
not
only
has
significant
impact
on
the
individual,
but
also
public
health
systems
national
economies.
Unfortunately,
there
no
single
standard
care
for
patients
with
LBP.
N-acetylcysteine
(NAC),
which
used
clinically
treat
acetaminophen
overdose,
recently
been
tested
as
potential
treatment
NAC
inexpensive
commercially
available,
it
an
established
tolerance
safety
profile.
However,
NAC's
efficacy
in
established.
This
scoping
review
presents
summary
studies
investigating
effects
benefits
treatment,
highlights
its
molecular
mechanisms
side
effects.
A
systematic
literature
search
Pubmed/MEDLINE,
Embase,
Scopus,
Science
Direct,
Web
Science,
Cinahl,
Lilacs
databases
was
conducted.
The
PRISMA-ScR
checklist
ensure
integrity
review.
protocol
registered
Open
Framework.
No
limit
set
study
language
publication
date.
In
total,
2357
articles
were
located,
16
included.
show
data
are
derived
from
few
clinical
trials
preclinical
studies.
Thus,
much
learn
more
should
be
performed
before
can
recommended
Cells,
Journal Year:
2025,
Volume and Issue:
14(8), P. 613 - 613
Published: April 19, 2025
Low
back
pain
is
a
widespread
condition
that
significantly
impacts
quality
of
life,
with
intervertebral
disc
degeneration
(IDD)
being
major
contributing
factor.
However,
the
underlying
mechanisms
IDD
remain
poorly
understood,
necessitating
further
investigation.
Environmental
risk
factors,
such
as
mechanical
stress
and
cigarette
smoke,
elevate
reactive
oxygen
species
levels
from
both
endogenous
exogenous
sources,
leading
to
redox
imbalance
oxidative
stress.
The
endoplasmic
reticulum
(ER)
mitochondria,
two
key
organelles
responsible
for
protein
folding
energy
production,
respectively,
are
particularly
vulnerable
Under
conditions,
ER
mitochondrial
dysfunction
occur,
resulting
in
unfolded
response
activation,
impaired
biosynthetic
processes,
disruptions
tricarboxylic
acid
cycle
electron
transport
chain,
ultimately
compromising
metabolism.
Prolonged
excessive
can
trigger
apoptosis
through
ER–mitochondrial
crosstalk.
Given
unique
microenvironment
(IVD)—characterized
by
hypoxia,
glucose
starvation,
region-specific
cellular
heterogeneity—the
differential
effects
environmental
stressors
on
distinct
IVD
cell
populations
require
This
review
explores
potential
which
factors
alter
activities,
progression,
discusses
future
therapeutic
strategies
aimed
at
mitigating
degeneration.