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.
Antioxidants and Redox Signaling,
Год журнала:
2025,
Номер
unknown
Опубликована: Март 17, 2025
Aims:
Myocardial
fibrosis
is
an
important
medium
for
atrial
fibrillation
(AF).
Exosomes
have
been
demonstrated
to
affect
the
development
of
AF.
This
study
explored
molecular
mechanism
exosomes
from
patients
with
AF
(AF-exo)
mediating
myocardial
and
thus
affecting
Results:
Prolactin-induced
protein
(PIP)
highly
expressed
in
AF-exo.
AF-exo
promoted
proliferation
activation
cardiac
fibroblasts
(CFs)
as
well
migration
endothelial-to-mesenchymal
transition
(EndMT)
human
umbilical
vein
endothelial
cells
(HUVECs).
However,
effect
on
CFs
HUVECs
was
mitigated
by
PIP-specific
short
hairpin
RNA
(shPIP).
Adeno-associated
virus
(AAV)-shPIP
reduced
incidence
duration
rats,
improved
collagen
deposition.
ATPase
plasma
membrane
Ca2+
transporting
2
(ATP2B2)
overexpression
or
inhibition
reverses
role
PIP
shPIP
CFs,
HUVECs,
rats.
Activation
cyclic
guanosine
monophosphate/protein
kinase
G
(cGMP/PKG)
pathway
beneficial
alleviate
fibrosis,
but
this
shATP2B2.
Innovation:
Our
investigation
substantiates
pivotal
PIP/ATP2B2
axis
both
HUVEC
EndMT
progression.
findings
suggest
that
can
suppress
cGMP/PKG
mediated
ATP2B2
through
exosomal
PIP,
promoting
indicating
potential
targets
novel
antifibrotic
drug
targeting
either
ATP2B2.
Conclusion:
Exosomal
inhibit
ATP2B2,
Antioxid.
Redox
Signal.
00,
000-000.
Frontiers in Endocrinology,
Год журнала:
2025,
Номер
16
Опубликована: Март 20, 2025
Tissue
fibrosis
represents
an
aberrant
repair
process,
occurring
because
of
prolonged
injury,
sustained
inflammatory
response,
or
metabolic
disorders.
It
is
characterized
by
excessive
accumulation
extracellular
matrix
(ECM),
resulting
in
tissue
hardening,
structural
remodeling,
and
loss
function.
This
pathological
phenomenon
a
common
feature
the
end
stage
numerous
chronic
diseases.
Despite
advent
novel
therapeutic
modalities,
including
antifibrotic
agents,
these
have
only
modest
efficacy
reversing
established
are
associated
with
adverse
effects.
In
recent
years,
growing
body
research
has
demonstrated
that
exercise
significant
benefits
potential
treatment
fibrosis.
The
anti-fibrotic
effects
mediated
multiple
mechanisms,
direct
inhibition
fibroblast
activation,
reduction
expression
pro-fibrotic
factors
such
as
transforming
growth
factor-β
(TGF-β)
slowing
collagen
deposition.
Furthermore,
been
to
assist
maintaining
dynamic
equilibrium
repair,
thereby
indirectly
reducing
damage
can
also
help
maintain
balance
improving
disorders,
exerting
anti-inflammatory
antioxidant
effects,
regulating
cellular
autophagy,
restoring
mitochondrial
function,
activating
stem
cell
activity,
apoptosis,
alleviating
tissue.
paper
presents
review
its
underlying
mechanisms
for
range
fibrosis,
cardiac,
pulmonary,
renal,
hepatic,
skeletal
muscle.
offers
valuable
reference
point
non-pharmacological
intervention
strategies
comprehensive
fibrotic
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.
Frontiers in Endocrinology,
Год журнала:
2025,
Номер
16
Опубликована: Апрель 7, 2025
Diabetic
cardiomyopathy
is
a
notable
microvascular
complication
of
diabetes,
characterized
primarily
by
myocardial
fibrosis
and
functional
abnormalities.
Long-term
hyperglycemia
induces
excessive
activation
recruitment
immune
cells
triggers
the
cascade
inflammatory
responses,
resulting
in
systemic
local
cardiac
inflammation.
Emerging
evidence
highlights
significant
roles
immunology
modulating
pathology
diabetic
cardiomyopathy.
As
primary
effectors
reactions,
are
consistently
present
tissue
can
be
recruited
under
pathological
circumstances.
A
disproportionate
favor
to
proinflammatory
types
increased
cytokine
levels
mediate
fibroblast
proliferation,
phenotypic
transformation,
collagen
synthesis
ultimately
rise
hypertrophy.
Meanwhile,
severity
also
strongly
associated
with
diverse
phenotypes
alterations
cells,
including
macrophages,
dendritic
mast
neutrophils,
natural
killer
innate
immunity
CD4+
T
lymphocytes,
CD8+
B
lymphocytes
adaptive
immunity.
In
this
review,
we
synthesized
current
analysis
critical
role
played
system
its
components
progression
Finally,
highlight
preclinical
clinical
targeting
strategies
translational
implications.
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.
