Frontiers in Immunology,
Год журнала:
2024,
Номер
15
Опубликована: Фев. 19, 2024
Background
Myocardial
infarction
(MI)
caused
by
severe
coronary
artery
disease
has
high
incidence
and
mortality
rates,
making
its
prevention
treatment
a
central
challenging
aspect
of
clinical
work
for
cardiovascular
practitioners.
Recently,
researchers
have
turned
their
attention
to
novel
mechanism
cell
death
Cu
2+
,
cuproptosis.
Methods
This
study
integrated
data
from
three
MI-related
bulk
datasets
downloaded
the
Gene
Expression
Omnibus
(GEO)
database,
identified
16
differentially
expressed
genes
(DEGs)
related
cuproptosis
taking
intersection
6378
DEGs
obtained
differential
analysis
with
49
cuproptosis-related
genes.
Four
hub
genes,
Dbt,
Dlat,
Ube2d1
Ube2d3,
were
screened
out
through
random
forest
Lasso
analysis.
In
group,
showed
low
expression,
while
Ube2d3
exhibited
expression.
Results
Focusing
on
subsequent
functional
studies,
we
confirmed
expression
in
MI
group
qRT-PCR
Western
Blot
detection
after
successful
construction
mouse
model
left
anterior
descending
(LAD)
ligation,
further
clarified
correlation
development
detecting
levels
proteins.
Moreover,
vitro
experiments,
was
be
highly
oxygen-glucose
deprivation
(OGD)-treated
cardiomyocytes
AC16.
order
clarify
role
knocked
down
OGD-treated
AC16
cells,
Ube2d3’s
promoting
hypoxia
damage
cells
inducing
cuproptosis,
as
evidenced
MTT,
TUNEL,
LDH
release
Conclusion
summary,
our
findings
indicate
that
regulates
affect
progression
MI.
Redox Biology,
Год журнала:
2024,
Номер
76, С. 103321 - 103321
Опубликована: Авг. 19, 2024
Cell
death
constitutes
a
critical
component
of
the
pathophysiology
cardiovascular
diseases.
A
growing
array
non-apoptotic
forms
regulated
cell
(RCD)-such
as
necroptosis,
ferroptosis,
pyroptosis,
and
cuproptosis-has
been
identified
is
intimately
linked
to
various
conditions.
These
RCD
are
governed
by
genetically
programmed
mechanisms
within
cell,
with
epigenetic
modifications
being
common
crucial
regulatory
method.
Such
include
DNA
methylation,
RNA
histone
acetylation,
non-coding
RNAs.
This
review
recaps
roles
modifications,
RNAs
in
diseases,
well
which
regulate
key
proteins
involved
death.
Furthermore,
we
systematically
catalog
existing
pharmacological
agents
targeting
novel
their
action
article
aims
underscore
pivotal
role
precisely
regulating
specific
pathways
thus
offering
potential
new
therapeutic
avenues
that
may
prove
more
effective
safer
than
traditional
treatments.
Journal of Inflammation Research,
Год журнала:
2025,
Номер
Volume 18, С. 251 - 270
Опубликована: Янв. 1, 2025
Background:
Lung
transplantation
is
the
only
effective
therapeutic
option
for
patients
with
end-stage
lung
disease.
However,
ischemia/reperfusion
injury
(IRI)
during
a
leading
cause
of
primary
graft
dysfunction
(PGD).
Ferroptosis,
form
iron-dependent
cell
death
driven
by
lipid
peroxidation,
has
been
implicated
in
IRI
across
various
organs.
This
study
aims
to
explore
role
ferroptosis
transplantation-related
and
identify
its
potential
molecular
mechanisms
through
bioinformatics
analysis.
Methods:
Transcriptome
data
from
transplant
were
obtained
Gene
Expression
Omnibus
(GEO)
database.
Ferroptosis-related
differentially
expressed
genes
(FRGs)
identified
analyzing
gene
expression
profiles
before
after
reperfusion.
Weighted
co-expression
network
analysis
(WGCNA)
was
used
module
genes,
overlapping
further
analyzed
using
two
machine
learning
algorithms.
The
CIBERSORT
algorithm
applied
assess
immune
infiltration,
while
Mendelian
randomization
(MR)
investigate
causal
relationships
between
candidate
PGD.
Finally,
Consensus
clustering
based
on
FRGs
performed
subtypes.
Results:
We
four
associated
reperfusion:
tumor
necrosis
factor
alpha-induced
protein
3
(TNFAIP3),
C-X-C
motif
chemokine
ligand
2
(CXCL2),
neural
precursor
developmentally
down-regulated
4-like
(NEDD4L),
sestrin
(SESN2).
These
closely
infiltration.
MR
suggested
that
SESN2
might
play
protective
against
Additionally,
consensus
revealed
distinct
infiltration
patterns
subtypes,
providing
insights
personalized
approaches
(LIRI).
Conclusion:
highlights
TNFAIP3,
CXCL2,
NEDD4L,
as
LIRI,
potentially
protecting
findings
offer
promising
targets
preventing
LIRI
improving
outcomes
transplantation.
Keywords:
injury,
ferroptosis,
biomarkers,
Frontiers in Cardiovascular Medicine,
Год журнала:
2025,
Номер
12
Опубликована: Март 31, 2025
Myocardial
infarction
(MI)
is
a
leading
cause
of
death
worldwide.
Immune
cells
play
significant
role
in
the
MI
development.
This
study
aims
to
identify
marker
related
neutrophil
for
diagnosis
and
early
progression
MI.
Key
genes
were
screened
using
three
machine
learning
algorithms
establish
diagnostic
model.
A
gene
associated
with
was
identified
based
on
single
cell
RNA
sequencing
data.
To
further
validate
predictive
value
gene,
mouse
models
constructed.
Immunofluorescence
(IF)
analysis
demonstrated
co-expression
neutrophils.
Immunohistochemistry
(IHC)
performed
Neutrophils
verified
as
key
infiltrating
immune
(IICs)
involved
onset
panel
superior
performance
developed
five
neutrophils
(AUC
=
0.887).
Among
panel,
IL1R2
found
phase
MI,
which
corroborated
by
IHC
suggests
that
IL1R2,
specific
neutrophils,
can
predict
providing
new
insights
into
clinical
management
Computers in Biology and Medicine,
Год журнала:
2023,
Номер
168, С. 107776 - 107776
Опубликована: Дек. 3, 2023
Amyotrophic
lateral
sclerosis
(ALS)
is
a
progressive
and
lethal
neurodegenerative
disease.
Several
studies
have
suggested
the
involvement
of
cuproptosis
in
its
pathogenesis.
In
this
research,
we
intend
to
explore
cuproptosis-related
molecular
clusters
ALS
develop
novel
genes
prediction
model.
Anti-Cancer Drugs,
Год журнала:
2024,
Номер
unknown
Опубликована: Май 3, 2024
Acute
myocardial
infarction
(AMI)
is
the
high
incidence
rate
and
mortality
of
common
cardiovascular
disease.
Herein,
we
explored
critical
role
TRIM11
in
AMI
its
underlying
mechanism.
Serum
from
patients
with
were
collected
our
hospital.
Mice
model
group
received
angiotensin
II.
+
Ang
II
vectors.
sham
normal
saline.
H9c2
cells
performed
transfections
using
Lipofectamine
2000
(Thermo
Fisher
Scientific
Inc,
Shanghai,
China),
treated
mRNA
expression
was
reduced,
negative
correlation
collagen
I/III
expression,
systolic
blood
pressure,
diastolic
left
anteroposterior
atrial
diameter,
right
or
ventricular
ejection
fraction
patient
AMI.
protein
also
suppressed.
METTL3
regulates
methylation
to
reduce
gene
stability
ameliorated
mice
model.
reduced
reactive
oxygen
species
production
level
cardiomyocyte
in-vitro
ferroptosis
by
inhibition
mitochondrial
damage
induced
Dusp6
expression.
Bioluminescence
imaging
showed
that
virus
increased
heart
tissue
The
effects
on
In
conclusion,
this
study
demonstrates
improves
regulating
inhibit
cardiomyocyte,
suggest
a
novel
target
for
iScience,
Год журнала:
2024,
Номер
27(7), С. 110275 - 110275
Опубликована: Июнь 14, 2024
Mitochondrial
dysfunction
has
been
known
to
contribute
the
worsening
of
acute
myocardial
infarction
(AMI).
We
screened
differentially
expressed
genes
(DEGs)
between
AMI
and
healthy
individuals
based
on
GSE66360
dataset.
took
intersection
obtained
DEGs
with
1,136
mitochondria-related
genes.
Finally,
we
out
(MitoDEGs).
Eight
MitoDEGs
were
identified
as
hub
random
forest
algorithm.
Two
robust
molecular
clusters
by
consensus
clustering.
Immune
infiltration
analysis
showed
that
immune
cell
was
significantly
increased
in
high-expression
group
MitoDEGs.
potential
drugs
targeted
at
