Advances in the study of S100A9 in cardiovascular diseases
Cell Proliferation,
Год журнала:
2024,
Номер
57(8)
Опубликована: Март 19, 2024
Abstract
Cardiovascular
disease
(CVD)
is
a
group
of
diseases
that
primarily
affect
the
heart
or
blood
vessels,
with
high
disability
and
mortality
rates,
posing
serious
threat
to
human
health.
The
causative
factors,
pathogenesis,
characteristics
common
CVD
differ,
but
they
all
involve
pathological
processes
such
as
inflammation,
oxidative
stress,
fibrosis.
S100A9
belongs
S100
family
calcium‐binding
proteins,
which
are
mainly
secreted
by
myeloid
cells
bind
Toll‐like
receptor
4
for
advanced
glycation
end
products
involved
in
regulating
inflammatory
response,
fibrosis,
vascular
calcification,
endothelial
barrier
function
CVD.
latest
research
has
found
key
biomarker
diagnosing
predicting
various
Therefore,
this
article
reviews
progress
on
diagnostic
predictive,
therapeutic
value
inflammatory‐related
atherosclerosis,
myocardial
infarction,
arterial
aneurysm
summarizes
its
molecular
mechanisms
progression
CVD,
aiming
explore
new
predictive
methods
identify
potential
intervention
targets
clinical
practice.
Язык: Английский
Role of S100A1, S100A4, S100A8/A9 and S100B in myocardial infarction and heart failure
International Immunopharmacology,
Год журнала:
2025,
Номер
151, С. 114348 - 114348
Опубликована: Март 1, 2025
Язык: Английский
Identification of regulator gene and pathway in myocardial ischemia-reperfusion injury: a bioinformatics and biological validation study
Hereditas,
Год журнала:
2025,
Номер
162(1)
Опубликована: Март 11, 2025
Abstract
Background
Acute
myocardial
infarction
(AMI)
is
the
primary
cause
of
cardiac
mortality
worldwide.
However,
ischemia-reperfusion
injury
(MIRI)
following
reperfusion
therapy
common
in
AMI,
causing
damage
and
affecting
patient’s
prognosis.
Presently,
there
are
no
effective
treatments
available
for
MIRI.
Methods
We
performed
a
comprehensive
bioinformatics
analysis
using
three
GEO
datasets
on
differentially
expressed
genes,
including
gene
ontology
(GO),
pathway
enrichment
analyses,
protein-protein
interaction
(PPI)
network
analysis.
Cytoscape
LASSO
methods
were
employed
to
identify
novel
regulator
genes
(I/R).
Notably,
S100A9
was
identified
as
potential
I/R.
Additionally,
clinical
sample
analyzed
prove
expression
mechanism
its
down
The
correlation
with
events
also
examined
enhance
reliability
our
results.
Results
135
differential
between
peripheral
blood
47
controls
92
I/R
patients.
distinguished
diagnostic
potential.
RT-qPCR
test
demonstrated
significant
upregulation
verified
that
strongly
correlates
left
ventricular
ejection
fraction
(LVEF)
Conclusion
This
study
confirms
key
progression
may
participate
by
upregulating
RAGE
/NFKB-NLRP3
activation.
Elevated
levels
serve
marker
identifying
high-risk
MIRI
patients,
especially
those
coronary
artery
no-reflow
(CNR),
who
might
benefit
from
targeted
therapeutic
interventions.
Furthermore,
Peripheral
AMI
represents
new
target
preventing
Язык: Английский
Semaglutide attenuates myocardial ischemia-reperfusion injury by inhibiting ferroptosis of cardiomyocytes via activation of PKC-S100A9 axis
Frontiers in Pharmacology,
Год журнала:
2025,
Номер
16
Опубликована: Март 20, 2025
Objective
The
incidence
of
ischemic
cardiomyopathy
increases
annually
worldwide,
and
it
is
the
leading
cause
mortality
in
China.
Although
interventional
diagnostic
therapeutic
techniques
can
promptly
open
culprit
vessels,
myocardial
ischemia-reperfusion
injury
(MIRI),
resulting
from
restored
blood
flow,
often
inevitable.
Semaglutide
(Sem),
a
novel
GLP-1
analogue,
primarily
utilized
managing
Type
2
diabetes
mellitus
(T2DM).
Recent
research
indicates
that
semaglutide
may
reduce
risk
major
adverse
cardiovascular
events.
Therefore,
purpose
this
study
to
explore
whether
ameliorate
MIRI
its
potential
mechanism.
Methods
results
:
A
mouse
model
(I/R)
was
created
by
ligating
left
anterior
descending
coronary
artery
(LAD)
first
for
45
min
then
reperfusing
heart
24
h.
Assessment
cardiac
function
fibrosis
were
conducted
through
small
animal
ultrasound
Masson’s
staining.
It
observed
enhanced
recovery
diminished
I/R
model.
In
vivo
experiments,
proved
mitigate
oxidative
stress
inhibit
ferroptosis
cardiomyocytes.
RNA
sequencing
showed
S100
calcium
binding
protein
A9
(S100A9)
target
gene
protect
against
MIRI.
vitro
,
experiments
decreased
expression
S100A9
activating
Protein
Kinase
C(PKC)
pathway,
thus
inhibiting
Conclusion
I/R-induced
mechanism,
mainly
via
activation
PKC
signaling
pathway.
considered
as
treatment
option
Язык: Английский
Comprehensive analysis of single-cell and bulk transcriptome unravels immune landscape of atherosclerosis and develops a S100 family based-diagnostic model
Computational Biology and Chemistry,
Год журнала:
2025,
Номер
unknown, С. 108436 - 108436
Опубликована: Март 1, 2025
Язык: Английский
The Identification of Key Genes and Biological Pathways in Cardiac Arrest by Integrated Bioinformatics and Next Generation Sequencing Data Analysis
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Авг. 19, 2024
Abstract
Cardiac
arrest
(CA)
is
a
common
cause
of
death
world
wide.
The
disease
has
lacks
effective
treatment.
Efforts
have
been
made
to
elucidate
the
molecular
pathogenesis
CA,
but
mechanisms
remain
elusive.
To
identify
key
genes
and
pathways
in
next
generation
sequencing
(NGS)
GSE200117
dataset
was
downloaded
from
Gene
Expression
Omnibus
(GEO)
database.
DESeq2
tool
used
recognize
differentially
expressed
(DEGs).
ontology
(GO)
REACTOME
pathway
enrichment
analyses
were
performed
analyze
DEGs
associated
signal
g:Profiler
IID
database
construct
protein-protein
interaction
(PPI)
network,
modules
analysis
using
Cytoscape.
A
miRNA-hub
gene
regulatory
network
TF-hub
then
constructed
screen
miRNAs,
TFs
hub
by
miRNet
NetworkAnalyst
Cityscape
software.
Receiver
operating
characteristic
curve
(ROC)
verified
genes.
In
total,
844
identified,
comprising
414
up
regulated
430
down
GO
indicated
that
for
CA
mainly
enriched
organonitrogen
compound
metabolic
process,
response
stimulus,
translation
immune
system.
Ten
(up-regulated:
HSPA8,
HOXA1,
INCA1
TP53;
down-regulated:
HSPB1,
LMNA,
SNCA,
ADAMTSL4
PDLIM7)
screened.
We
also
predicted
miRNAs
(hsa-mir-1914-5p
hsa-mir-598-3p)
(JUN
PRRX2)
targeting
This
study
uses
series
bioinformatics
technologies
obtain
hug
genes,
TFs,
related
CA.
These
results
provide
us
with
new
ideas
finding
biomarkers
treatment
methods
Язык: Английский