Epithelial
Ovarian
Cancer
(EOC)
is
complex
and
heterogeneous,
making
accurate
prognosis
treatment
prediction
difficult.
New
therapeutic
targets
their
mechanisms
are
urgently
needed.
This
study
explored
the
role
of
PTTG1
in
ovarian
cancer
via
cGMP-PKG
signaling
pathway,
focusing
on
its
effects
M2
macrophage
polarization
EMT
progression
EOC
cells.
Using
GSE135886
database,
we
performed
differential
gene
expression,
pathway
enrichment,
immune
infiltration
analyses
to
identify
key
influencing
polarization.
We
then
constructed
knockdown
overexpression
cell
lines
assess
impact
proliferation,
migration,
invasion,
EMT,
vitro.
Analysis
revealed
that
differentially
expressed
genes
were
enriched
correlated
with
macrophages.
A2780
SK-OV-3
cells
promoted
while
enhancing
sGC,
PKG1,
PKG2
expression
activate
induce
produced
opposite
results,
reinforcing
our
conclusions.
uncovers
a
novel
mechanism
development
suggests
it
as
potential
target.
International Journal of Cardiology Cardiovascular Risk and Prevention,
Год журнала:
2024,
Номер
24, С. 200355 - 200355
Опубликована: Дек. 6, 2024
Cardiovascular
diseases
(CVDs),
such
as
atherosclerotic
cardiovascular
diseases,
heart
failure
(HF),
and
acute
coronary
syndrome,
represent
a
significant
threat
to
global
health
impose
considerable
socioeconomic
burdens.
The
intricate
pathogenesis
of
CVD
involves
various
regulatory
mechanisms,
among
which
microRNAs
(miRNAs)
have
emerged
critical
posttranscriptional
regulators.
In
particular,
miR-155
has
demonstrated
differential
expression
patterns
across
spectrum
is
implicated
in
the
etiology
progression
arterial
disorders.
This
systematic
review
synthesizes
current
evidence
on
multifaceted
roles
modulation
genes
pathological
processes
associated
with
CVD.
We
delineate
potential
diagnostic
biomarker
therapeutic
target,
highlighting
its
influence
conditions
atherosclerosis,
aneurysm,
hypertension,
HF,
myocardial
hypertrophy,
oxidative
stress.
Our
analysis
underscores
transformative
target
for
intervention
medicine,
warranting
further
investigation
into
clinical
applicability.
Acute
myocardial
infarction
(AMI)
is
a
serious
cardiovascular
disease
for
which
there
are
still
no
effective
therapeutic
options
available,
and
melanoma-associated
antigen-A13
(Magea13),
member
of
the
MAGE
superfamily,
has
an
unknown
role
in
AMI.
This
study
aims
to
investigate
potential
molecular
mechanisms
Magea13
injury
associated
with
AMI
through
vivo
vitro
experiments.
Firstly,
differentially
expressed
genes
(DEGs)
signaling
pathways
were
screened
by
RNA
sequencing.
Cardiac-specific
overexpression
was
achieved
adeno-associated
virus
type
9
serotype
system.
Subsequently,
these
rats
underwent
left
anterior
descending
coronary
artery
(LAD)
ligation,
followed
histopathological
examination,
biochemical
assay,
Western
blot
analysis
evaluate
efficacy
feasibility
Meanwhile,
Magea13-overexpressing
rat
cardiomyocyte
cell
line
(H9c2)
also
subjected
hypoxia-glucose
deficiency/reperfusion
mimic
further
validate
its
effects
vitro.
The
cardiomyocyte-specific
observed
attenuate
acute
infarction.
Furthermore,
demonstrated
OGD/R-induced
H9c2
injury.
Mechanistic
studies
have
suggested
that
protective
effect
may
be
mediated
cAMP-PKA
pathway.
been
offer
protection
against
pathway
therefore
promising
predictive
target
Circulation Research,
Год журнала:
2025,
Номер
136(7), С. 773 - 802
Опубликована: Март 27, 2025
Cardiac
fibrosis,
a
hallmark
of
heart
failure
and
various
cardiomyopathies,
represents
complex
pathological
process
that
has
long
challenged
therapeutic
intervention.
High-throughput
omics
technologies
have
begun
revolutionizing
our
understanding
the
molecular
mechanisms
driving
cardiac
fibrosis
are
providing
unprecedented
insights
into
its
heterogeneity
progression.
This
review
provides
comprehensive
analysis
how
techniques—encompassing
genomics,
epigenomics,
transcriptomics,
proteomics,
metabolomics—are
insight
fibrosis.
Genomic
studies
identified
novel
genetic
variants
regulatory
networks
associated
with
susceptibility
progression,
single-cell
transcriptomics
unveiled
distinct
fibroblast
subpopulations
unique
signatures.
Epigenomic
profiling
revealed
dynamic
chromatin
modifications
controlling
activation
states,
proteomic
analyses
biomarkers
potential
targets.
Metabolomic
uncovered
important
alterations
in
energetics
substrate
utilization
during
fibrotic
remodeling.
The
integration
these
multi-omic
data
sets
led
to
identification
previously
unrecognized
pathogenic
targets,
including
cell-type-specific
interventions
metabolic
modulators.
We
discuss
advances
development
precision
medicine
approaches
for
while
highlighting
current
challenges
future
directions
translating
effective
strategies.
systems-level
perspective
on
may
inform
more
effective,
personalized
related
cardiovascular
diseases.
Epithelial
Ovarian
Cancer
(EOC)
is
complex
and
heterogeneous,
making
accurate
prognosis
treatment
prediction
difficult.
New
therapeutic
targets
their
mechanisms
are
urgently
needed.
This
study
explored
the
role
of
PTTG1
in
ovarian
cancer
via
cGMP-PKG
signaling
pathway,
focusing
on
its
effects
M2
macrophage
polarization
EMT
progression
EOC
cells.
Using
GSE135886
database,
we
performed
differential
gene
expression,
pathway
enrichment,
immune
infiltration
analyses
to
identify
key
influencing
polarization.
We
then
constructed
knockdown
overexpression
cell
lines
assess
impact
proliferation,
migration,
invasion,
EMT,
vitro.
Analysis
revealed
that
differentially
expressed
genes
were
enriched
correlated
with
macrophages.
A2780
SK-OV-3
cells
promoted
while
enhancing
sGC,
PKG1,
PKG2
expression
activate
induce
produced
opposite
results,
reinforcing
our
conclusions.
uncovers
a
novel
mechanism
development
suggests
it
as
potential
target.
