ESC Heart Failure,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Nov. 6, 2024
Abstract
Aims
Inflammation
plays
a
critical
role
in
both
the
development
and
progression
of
heart
failure
(HF),
which
is
leading
cause
morbidity
mortality
worldwide.
However,
causality
between
specific
inflammation‐related
proteins
HF
risk
remains
unclear.
This
study
aims
to
investigate
genetically
supported
inflammatory
using
two‐sample
Mendelian
randomization
(MR)
analysis.
Methods
results
We
utilized
genome‐wide
association
(GWAS)
data
91
as
exposures
from
SCALLOP
Consortium
(14,824
participants),
alongside
outcome
GWAS
summary
statistics
FinnGen
(29,218
cases/381,838
controls)
HERMES
(47,309
cases/930,014
for
HF,
conduct
MR
For
each
protein,
instrumental
variables
(IVs)
were
chosen
following
three
foundational
assumptions
analysis,
requiring
minimum
qualifying
single
nucleotide
polymorphisms
(SNPs)
with
P
<
5e‐8.
Associations
assessed
through
inverse‐variance
weighted
(IVW),
MR‐Egger
regression,
median
mode
The
reliability
validity
evaluated
by
examining
heterogeneity,
horizontal
pleiotropy,
leave‐one‐out
meta‐analysis
reverse
Heterogeneity
refers
variation
across
different
genetic
variants.
Horizontal
pleiotropy
occurs
when
variant
influences
multiple
traits
biological
pathways.
Addressing
heterogeneity
crucial
ensuring
interpretability
results.
Our
analysis
identified
associations
risk.
Matrix
metalloproteinase‐1
(MMP‐1)
(OR,
1.09;
95%
CI,
1.00–1.18;
=
0.04)
TNF‐beta
1.05;
1.01–1.09;
0.01)
positively
associated
FinnGen.
In
contrast,
urokinase‐type
plasminogen
activator
(uPA)
was
inversely
0.85;
0.78–0.92;
3.27e‐5)
0.93;
0.87–0.99;
0.03).
No
evidence
observed
indicating
robustness
our
findings.
A
further
this
association,
reduced
0.89;
0.81–0.98;
0.02).
found
these
(
>
0.05
all).
Conclusions
provides
causal
positive
MMP‐1
suggests
their
roles
disease
pathogenesis,
whereas
inverse
uPA
indicates
its
potential
protective
effect.
findings
highlight
targeting
pathways
therapeutic
strategy
HF.
Reviews in Cardiovascular Medicine,
Journal Year:
2025,
Volume and Issue:
26(2)
Published: Feb. 21, 2025
Background:
Fibulin
1
and
2
are
members
of
the
extracellular
matrix
(ECM)
glycoprotein
family.
ECMs
drive
prognosis
through
remodeling,
a
key
step
in
pathogenesis
heart
failure
(HF).
We
aimed
to
compare
levels
different
stages
HF
investigate
their
relationship
with
other
prognostic
factors
HF.
Methods:
Patients
were
divided
into
two
groups
according
left
ventricular
ejection
fraction
(LVEF):
reduced
non-reduced
LVEF.
The
control
patient
consisted
individuals
Stages
A
B
HF,
C
D
respectively.
measured
at
group.
Additionally,
admission,
discharge,
first
month
patients
who
hospitalized
due
decompensated
Results:
Serum
N-terminal
pro-B-type
natriuretic
peptide
(NT-proBNP)
significantly
higher
group
than
similar
between
groups.
Although
serum
repeated
measurements,
NT-proBNP
decreased
discharge
remained
compared
admission.
There
was
significant
positive
correlation
negative
not
correlated
LVEF
NT-proBNP.
Conclusions:
Our
study
demonstrated
that
differ
among
have
temporal
change
as
observed
for
levels.
association
our
study.
Cureus,
Journal Year:
2025,
Volume and Issue:
unknown
Published: March 27, 2025
Cardiac
fibrosis,
characterized
by
excessive
extracellular
matrix
deposition,
contributes
to
heart
failure,
arrhythmias,
and
myocardial
dysfunction.
Despite
advances
in
understanding
its
mechanisms,
targeted
antifibrotic
therapies
remain
limited.
This
review
examines
the
causes,
molecular
diagnostic
approaches,
therapeutic
strategies
for
cardiac
fibrosis.
A
systematic
of
peer-reviewed
studies
was
conducted,
focusing
on
etiology,
diagnosis,
treatment,
prognosis
fibrosis
with
no
specific
timeframe.
The
condition
is
driven
fibroblast
activation,
inflammatory
pathways,
mechanical
stress,
key
contributing
factors
including
ischemic
disease,
hypertension,
diabetes,
aging.
Diagnostic
tools
such
as
magnetic
resonance
imaging
T1
mapping
biomarkers
play
a
crucial
role,
natriuretic
peptides
offering
both
prognostic
value.
Galectin-3
has
also
shown
promise
marker.
Current
therapies,
RAAS
inhibitors
beta-blockers,
help
prevent
progression
but
do
not
reverse
established
Emerging
plant-based
compounds,
gene
therapy,
fibroblast-targeting
vaccines,
stem
cell
reprogramming
show
potential
preclinical
studies.
However,
remains
major
driver
disease
progression,
existing
treatments
Major
gaps
include
lack
validated
agents
challenges
translating
findings
into
clinical
applications.
Further
research
essential
develop
effective
interventions.
Advanced Healthcare Materials,
Journal Year:
2024,
Volume and Issue:
13(21)
Published: March 27, 2024
Fibrosis,
which
is
primarily
marked
by
excessive
extracellular
matrix
(ECM)
deposition,
a
pathophysiological
process
associated
with
many
disorders,
ultimately
leads
to
organ
dysfunction
and
poor
patient
outcomes.
Despite
the
high
prevalence
of
fibrosis,
currently
there
exist
few
therapeutic
options,
importantly,
paucity
in
vitro
models
accurately
study
fibrosis.
This
review
discusses
multifaceted
nature
fibrosis
from
viewpoint
developing
organ-on-chip
(OoC)
disease
models,
focusing
on
five
key
features:
ECM
component,
inflammation,
mechanical
cues,
hypoxia,
vascularization.
The
potential
OoC
technology
explored
for
better
modeling
these
features
context
studying
fibrotic
diseases
interplay
between
various
emphasized.
paper
reviews
how
organ-specific
are
modeled
platforms,
elements
included
existing
avenues
novel
research
directions
highlighted.
Finally,
this
concludes
perspective
address
current
gap
respect
inclusion
multiple
yield
more
sophisticated
relevant
an
format.
Biomedicine & Pharmacotherapy,
Journal Year:
2024,
Volume and Issue:
179, P. 117367 - 117367
Published: Aug. 29, 2024
The
pyroptosis
of
cardiomyocytes
has
become
an
essential
topic
in
heart
failure
research.
abnormal
accumulation
these
biological
factors,
including
angiotensin
II,
advanced
glycation
end
products,
and
various
growth
factors
(such
as
connective
tissue
factor,
vascular
endothelial
transforming
factor
beta,
among
others),
activates
the
nuclear
factor-κB
(NF-κB)
signaling
pathway
cardiovascular
diseases,
ultimately
leading
to
cardiomyocytes.
Therefore,
exploring
underlying
molecular
mechanisms
is
for
developing
novel
drugs
therapeutic
strategies.
However,
our
current
understanding
precise
regulatory
mechanism
this
complex
cardiomyocyte
still
limited.
Given
this,
study
reviews
milestone
discoveries
field
research
since
1986,
analyzes
detail
similarities,
differences,
interactions
between
other
cell
death
modes
apoptosis,
necroptosis,
autophagy,
ferroptosis),
explores
deep
connection
failure.
At
same
time,
it
depicts
complete
activation,
transmission,
eventual
NF-κB
process
In
addition,
also
systematically
summarizes
approaches
that
can
inhibit
reduce
pyroptosis,
drugs,
natural
compounds,
small
molecule
inhibitors,
gene
editing,
cutting-edge
technologies,
aiming
provide
solid
scientific
support
new
perspectives
prevention
treatment
Heart,
Journal Year:
2024,
Volume and Issue:
110(19), P. 1157 - 1163
Published: Aug. 7, 2024
Myocardial
remodelling,
entailing
cellular
and
molecular
changes
in
the
different
components
of
cardiac
tissue
response
to
damage,
underlies
morphological
structural
leading
which
turn
contributes
dysfunction
disease
progression.
Since
is
not
available
for
histomolecular
diagnosis,
surrogate
markers
are
needed
evaluating
myocardial
remodelling
as
part
clinical
management
patients
with
disease.
In
this
setting,
circulating
biomarkers,
a
component
liquid
biopsy,
provide
promising
approach
fast,
affordable
scalable
screening
large
numbers
patients,
allowing
detection
pathological
features
related
aiding
risk
stratification
therapy
monitoring.
However,
despite
advances
field
identification
numerous
potential
candidates,
their
implementation
practice
beyond
natriuretic
peptides
troponins
mostly
lacking.
review,
we
will
discuss
some
biomarkers
alterations
main
compartments
(cardiomyocytes,
extracellular
matrix,
endothelium
immune
cells)
have
shown
assessment
cardiovascular
risk,
effects.
The
hurdles
challenges
translation
into
also
be
addressed.
