Ecdysterone Alleviates Atherosclerosis by Inhibiting NCF2 and Inhibiting Ferroptosis Mediated by the PI3K/Akt/Nrf2 Pathway
Zhenyu Wang,
No information about this author
Fengchao Wu,
No information about this author
Yan Ju
No information about this author
et al.
Journal of Cellular and Molecular Medicine,
Journal Year:
2025,
Volume and Issue:
29(5)
Published: March 1, 2025
Ecdysterone
(Ecd),
an
active
ingredient
in
trianthema,
has
a
strong
anti-inflammatory
effect.
This
study
aimed
to
explore
the
potential
mechanism
by
which
Ecd
improves
atherosclerosis
(AS).
Here,
we
systematically
investigated
of
human
umbilical
vein
endothelial
cells
(HUVECs)
treated
with
oxidised
low-density
lipoprotein
(ox-LDL).
In
ox-LDL-treated
HUVECs,
promoted
HUVEC
viability
as
well
inhibited
ferroptosis
and
secretion
inflammatory
factors
(TNF-α,
IL-6
IL-1β).
addition,
expression
neutrophil
cytoplasmic
factor
2
(NCF2)
triggered
PI3K/AKT/Nrf2
signalling
pathway,
thereby
alleviating
increase
HUVECs.
More
importantly,
constructed
AS
mouse
model
feeding
ApoE-/-
mice
high-fat
diet
found
that
treatment
alleviated
vasculopathy
arterial
vivo,
could
be
reversed
overexpression
NCF2.
Overall,
this
showed
protective
effect
on
is
mainly
achieved
inhibiting
NCF2
activating
PI3K/Akt/Nrf2
pathway
inhibit
ferroptosis.
Therefore,
may
effective
drug
improve
ferroptosis-induced
inflammation.
Language: Английский
Exploring the Therapeutic Potential of MIR‐140‐3p in Osteoarthritis: Targeting CILP and Ferroptosis for Novel Treatment Strategies
Feng Ma,
No information about this author
Lexin Wang,
No information about this author
Hao Chi
No information about this author
et al.
Cell Proliferation,
Journal Year:
2025,
Volume and Issue:
unknown
Published: March 5, 2025
Osteoarthritis
(OA)
is
a
prevalent
and
debilitating
joint
disorder
that
affects
millions
of
individuals
worldwide,
severely
impairing
mobility,
independence,
quality
life.
Emerging
evidence
suggests
ferroptosis
critical
factor
in
OA
pathogenesis.
However,
its
precise
involvement
underlying
mechanisms
remain
poorly
understood.
In
this
study,
we
first
identified
cartilage
intermediate
layer
protein
(CILP)
mediates
the
regulation
ferroptosis-related
genes
through
hdWGCNA
analysis
combined
with
single-cell
RNA
sequencing.
Further
investigation
revealed
significant
upregulation
CILP
expression
C28/I2
cells
under
LPS
induction.
Mechanistically,
bioinformatics
differentially
expressed
miRNAs;
qRT-PCR
dual-luciferase
experiment
miR-140-3p
was
downregulated
directly
targets
CILP.
Experimental
data
further
demonstrated
regulates
ferroptosis,
inflammation,
oxidative
stress
by
targeting
These
findings
offer
valuable
insights
into
molecular
miR-140-3p/CILP
axis
regulating
stress,
thus
providing
foundation
for
developing
therapeutic
strategies
OA.
Language: Английский
Bioinformatics analysis techniques identify the ferroptosis-related gene MYC as a potential therapeutic target for spinal cord injury: an observational study based on the GEO database
Xiaowei Zha
No information about this author
Advanced technology in neuroscience .,
Journal Year:
2025,
Volume and Issue:
2(2), P. 59 - 71
Published: April 8, 2025
JOURNAL/atin/04.03/02274269-202506000-00001/figure1/v/2025-04-06T104049Z/r/image-tiff
Spinal
cord
injury
is
a
destructive
disease
with
limited
effective
treatment
options.
Ferroptosis,
form
of
regulated
cell
death,
has
been
suggested
to
be
related
the
pathogenesis
spinal
injury.
This
study
aimed
elucidate
prognostic
value
and
therapeutic
potential
ferroptosis-related
genes
in
using
advanced
bioinformatics
techniques.
We
retrieved
datasets
from
GEO
database
identified
differentially
expressed
between
control
groups.
These
were
intersected
identify
genes.
A
hub
gene
was
through
cytoHubba
plugin
Cytoscape,
miRNA–mRNA–transcription
factor
drug–biomarker
networks
constructed
reveal
molecular
targets
compounds.
The
results
revealed
highly
upregulated
gene,
MYC
,
group.
Subsequent
analyses
30
miRNAs,
transcription
factors,
drugs
as
associated
this
for
findings
suggest
that
analysis
techniques
provide
new
insights
into
role
injury,
highlighting
biomarker
target
lays
foundation
personalized
facilitating
development
strategies
tailored
unique
characteristics
individual
patients.
Language: Английский
ADORA2B promotes proliferation and migration in head and neck squamous cell carcinoma and is associated with immune infiltration
Pian Li,
No information about this author
Kai Pang,
No information about this author
Shuanghui Chen
No information about this author
et al.
BMC Cancer,
Journal Year:
2025,
Volume and Issue:
25(1)
Published: April 12, 2025
Adenosine
A2B
receptor
(ADORA2B),
a
G
protein-coupled
receptor,
is
implicated
in
tumor
progression
and
immune
regulation
various
cancers.
However,
its
specific
role
head
neck
squamous
cell
carcinoma
(HNSC)
remains
largely
unexplored.
This
study
aims
to
elucidate
the
expression
profile,
prognostic
value,
modulatory
role,
therapeutic
potential
of
ADORA2B
HNSC.
Comprehensive
bioinformatics
analyses
were
performed
using
TCGA
GEO
datasets
evaluate
expression,
clinical
correlations,
significance
Weighted
gene
co-expression
network
analysis
(WGCNA)
functional
enrichment
conducted
explore
ADORA2B-associated
pathways.
Immune
infiltration
was
assessed
via
ESTIMATE
single-sample
set
(ssGSEA).
checkpoint
blockade
(ICB)
therapy
sensitivity
drug
analyzed
IMvigor210
NCI-60
databases,
respectively.
In
vitro
experiments,
including
siRNA-mediated
knockdown,
CCK-8
assays,
colony
formation,
wound
healing
validate
oncogenic
ADORA2B.
significantly
overexpressed
HNSC
tissues
compared
adjacent
normal
tissues,
correlated
with
advanced
stage
as
well
poor
overall
survival
(OS)
progression-free
(PFS).
Functional
revealed
significant
downregulation
immune-related
pathways
high
groups.
High
associated
more
immunosuppressive
microenvironment
(TME),
characterized
by
lower
stromal
scores
reduced
infiltration.
Immunotherapy
response
demonstrated
that
patients
exhibited
poorer
outcomes
following
ICB
therapy.
Drug
identified
several
agents,
Ixazomib
citrate,
Masitinib,
others,
candidates
for
patients.
experiments
confirmed
knockdown
inhibited
proliferation,
migration,
underscoring
critical
progression.
key
driver
HNSC,
contributing
an
TME.
Its
prognosis
immunotherapy
efficacy.
Targeting
may
enhance
overcome
treatment
resistance,
highlighting
diagnostic,
prognostic,
biomarker.
Language: Английский
Identification of Therapeutic Targets for Hyperuricemia: Systematic Genome-Wide Mendelian Randomization and Colocalization Analysis
Na Chen,
No information about this author
Leilei Gong,
No information about this author
Li Zhang
No information about this author
et al.
Biomedicines,
Journal Year:
2025,
Volume and Issue:
13(5), P. 1022 - 1022
Published: April 23, 2025
Background:
At
present,
there
are
still
limitations
and
challenges
in
the
treatment
of
hyperuricemia
(HUA).
Mendelian
randomization
(MR)
has
been
widely
used
to
identify
new
therapeutic
targets.
Therefore,
we
conducted
a
systematic
druggable
genome-wide
MR
explore
potential
targets
drugs
for
HUA.
Methods:
We
integrated
genome
data;
blood,
kidney,
intestinal
expression
quantitative
trait
loci
(eQTLs);
HUA-associated
association
study
(GWAS)
data
analyze
causal
relationships
between
drug
target
genes
HUA
using
method.
Summary-data-based
(SMR)
analysis
Bayesian
colocalization
were
assess
causality.
In
addition,
phenome-wide
studies,
protein
network
construction,
enrichment
significant
evaluate
their
biological
functions
side
effects.
Finally,
performed
prediction
molecular
docking
targeting
these
treatment.
Results:
Overall,
identified
22
significantly
associated
with
through
MR,
SMR,
analyses.
Among
them,
two
prior
(ADORA2B
NDUFC2)
reached
statistically
levels
at
least
tissues
intestine.
Further
results
from
studies
revealed
that
no
effects
ADORA2B
or
NDUFC2.
Moreover,
screened
15
could
serve
as
candidates
development.
Conclusions:
This
provides
genetic
evidence
supporting
benefits
treatment,
offering
insights
into
development
targeted
Language: Английский
To verify the biological characteristics of disulfidptosis associated gene ADORA2B in esophageal cancer
Yixiao Cui,
No information about this author
Yuhan Deng,
No information about this author
Zhenhua Wu
No information about this author
et al.
BMC Gastroenterology,
Journal Year:
2025,
Volume and Issue:
25(1)
Published: May 19, 2025
Language: Английский
Battling pain from osteoarthritis: causing novel cell death
Yuheng Zhang,
No information about this author
Huaqiang Tao,
No information about this author
Liyuan Zhang
No information about this author
et al.
Acta Biochimica et Biophysica Sinica,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Oct. 1, 2024
Osteoarthritis
(OA)
is
a
significant
contributor
to
pain
and
disability
worldwide.
Pain
the
main
complaint
of
OA
patients
attending
clinic
has
large
impact
on
their
quality
life
economic
standards.
However,
existing
treatments
for
OA-related
have
not
been
shown
achieve
good
relief.
The
focus
preventing
slowing
progression
so
that
problem
can
be
resolved.
caused
by
complex,
with
nature,
location,
duration,
intensity
changing
as
disease
progresses.
Previous
research
highlighted
role
various
forms
cell
death,
such
apoptosis
necrosis,
in
OA.
Emerging
studies
identified
additional
novel
pyroptosis,
ferroptosis,
necroptosis
are
linked
Different
types
death
contribute
tissue
damage
impacting
inflammatory
responses,
reactive
oxygen
species
(ROS)
production,
calcium
ion
levels,
ultimately
leading
development
pain.
Evidence
suggests
targeting
could
help
alleviate
patients.
This
review
delves
into
complex
mechanisms
pain,
explores
relationship
between
different
modes
proposes
viable
strategy
treatment
these
conditions,
goal
providing
scientific
references
future
drugs.
Language: Английский