Phytomedicine,
Journal Year:
2024,
Volume and Issue:
127, P. 155467 - 155467
Published: Feb. 19, 2024
The
death
and
disability
caused
by
myocardial
infarction
is
a
health
problem
that
needs
to
be
addressed
worldwide,
poor
cardiac
repair
fibrosis
after
seriously
affect
patient
recovery.
Postmyocardial
M2
macrophages
of
great
significance
for
ventricular
remodeling.
Quercitrin
(Que)
common
flavonoid
in
fruits
vegetables
has
antioxidant,
anti-inflammatory,
antitumor
other
effects,
but
whether
it
role
the
treatment
unclear.
In
this
study,
we
constructed
mouse
model
administered
Que.
We
found
through
ultrasound
Que
administration
improved
ejection
fraction
reduced
Staining
heart
sections
detection
marker
protein
levels
revealed
slowed
infarction.
Flow
cytometry
showed
proportion
was
increased
expression
macrophage
markers
were
Que-treated
group.
Finally,
identified
metabolomics
reduces
glycolysis,
increases
aerobic
phosphorylation,
alters
arginine
metabolic
pathways,
polarizing
toward
phenotype.
Our
research
lays
foundation
future
application
cardiovascular
diseases.
Redox Biology,
Journal Year:
2024,
Volume and Issue:
71, P. 103109 - 103109
Published: March 1, 2024
Cardiac
fibrosis
is
a
major
public
health
problem
worldwide,
with
high
morbidity
and
mortality,
affecting
almost
all
patients
heart
disease
worldwide.
It
characterized
by
fibroblast
activation,
abnormal
proliferation,
excessive
deposition,
distribution
of
extracellular
matrix
(ECM)
proteins.
The
maladaptive
process
cardiac
complex
often
involves
multiple
mechanisms.
With
the
increasing
research
on
fibrosis,
redox
has
been
recognized
as
an
important
part
remodeling,
imbalance
in
homeostasis
can
adversely
affect
function
structure
heart.
metabolism
metal
ions
essential
for
life,
cells
impair
variety
biochemical
processes,
especially
redox.
However,
current
ion
still
very
limited.
This
review
comprehensively
examines
effects
(iron,
copper,
calcium,
zinc)
metabolism-mediated
outlines
possible
therapeutic
interventions,
addresses
ongoing
challenges
this
rapidly
evolving
field.
Biomedicines,
Journal Year:
2025,
Volume and Issue:
13(2), P. 259 - 259
Published: Jan. 21, 2025
Background/Objectives:
ST-segment
elevation
acute
coronary
syndrome
(STE-ACS)
represents
a
significant
global
health
challenge,
with
cardiac
remodeling
and
fibrosis
critically
affecting
recovery
after
percutaneous
intervention
(PCI).
Colchicine,
known
for
its
anti-inflammatory
effects,
may
regulate
key
fibrotic
markers
such
as
Procollagen
III
N-terminal
Propeptide
(PIIINP)
Galectin-3.
This
study
assesses
colchicine’s
effect
on
these
biomarkers
in
STE-ACS
patients
undergoing
delayed
PCI.
Methods:
In
this
multicenter,
randomized,
double-blind
trial,
we
examined
impact
Galectin-3
PIIINP
164
early
or
Patients
received
colchicine
shortly
hospital
admission.
Biomarker
changes
were
evaluated
at
24
h
five
days
post-treatment
using
two-way
ANOVA.
Results:
Clinical
trials
the
PCI
group
revealed
that
levels
decreased
significantly
day
one
(p
<
0.01)
further
0.0001),
indicating
Primary
has
benefits
to
inhibition
of
beyond
add-on
treatment.
But,
group,
increased
0.01),
but
decrease
observed
by
was
not
statistically
significant.
It
is
related
treatment
exceed
implantation
preventing
remodeling.
showed
reduction
0.0001).
Conclusions:
Colchicine
demonstrates
novel
efficacy
PCI,
increase
sharp
PIIINP,
ability
control
fibrosis.
positions
breakthrough
therapy
improving
outcomes
intervention.
International Immunopharmacology,
Journal Year:
2025,
Volume and Issue:
146, P. 113710 - 113710
Published: Jan. 1, 2025
Chronic
heart
failure,
caused
by
myocardial
fibrosis
after
acute
infarction
(AMI),
remains
a
serious
clinical
problem
that
needs
urgent
resolution.
Nitro-oleic
acid
(OA-NO2),
an
electrophilic
nitro-fatty
found
in
human
plasma,
is
believed
to
regulate
various
pathophysiological
functions,
particularly
anti-inflammation
and
anti-fibrosis.
However,
the
role
of
OA-NO2
AMI
unexplored.
Thus,
our
aim
was
investigate
whether
could
ameliorate
post-myocardial
fibrosis,
improve
cardiac
function,
elucidate
its
mechanism
mice.
In
vivo
experiments
involved
constructing
mice
model
administering
via
subcutaneous
osmotic
minipumps.
Echocardiography
transmission
electron
microscope
indicated
can
alleviate
injury
systolic
function.
Transcriptomics
tissue
suggested
improved
fibrosis.
Immunohistochemistry
qPCR
results
demonstrated
OA-NO2's
reduction
accumulation
extracellular
matrix
(Collagen
I
Collagen
III).
vitro
showed
remarkably
suppressed
activation
fibroblasts
myofibroblast
transition
induced
transforming
growth
factor-β
(TGF-β).
Furthermore,
inhibited
expression
α-SMA,
collagen
I,
III
TGF-β/smad2/3
signaling
pathway.
Immunofluorescence
ELISA
detection
revealed
not
only
alleviated
but
also
reduced
inflammation
decreased
inflammatory
factors
(TNF-α,
IL-1β,
IL-6,
MCP-1).
Mechanistically,
significantly
polarization
LPS-induced
macrophages
into
M1-type
inhibiting
NF-κB
(P65)
related
pathways.
Therefore,
postmyocardial
function
myofibroblasts
M1
macrophages.
Frontiers in Pharmacology,
Journal Year:
2025,
Volume and Issue:
16
Published: March 20, 2025
Aging
is
an
independent
risk
factor
for
many
chronic
diseases,
including
cancer
and
cardiovascular,
pulmonary,
neurodegenerative
diseases.
In
recent
years,
the
mechanisms
of
aging-related
cardiovascular
diseases
(CVDs)
have
been
studied
intensively.
Takeda
G
protein-coupled
receptor
5
(TGR5)
a
membrane
bile
acids
that
has
found
to
play
important
role
in
various
disease
processes,
such
as
inflammation,
oxidative
stress,
metabolic
disorders,
all
which
contribute
CVDs.
this
review,
we
summarise
TGR5
CVDs
propose
attractive
therapeutic
target
based
on
its
mechanism
involvement,
may
future
drug
design.
Current Issues in Molecular Biology,
Journal Year:
2024,
Volume and Issue:
46(3), P. 2181 - 2208
Published: March 8, 2024
Despite
improvements
in
contemporary
medical
and
surgical
therapies,
cardiovascular
disease
(CVD)
remains
a
significant
cause
of
worldwide
morbidity
mortality;
more
specifically,
ischemic
heart
(IHD)
may
affect
individuals
as
young
20
years
old.
Typically
managed
with
guideline-directed
therapy,
interventional
or
methods,
the
incurred
cardiomyocyte
loss
is
not
always
completely
reversible;
however,
recent
research
into
various
stem
cell
(SC)
populations
has
highlighted
their
potential
for
treatment
perhaps
regeneration
injured
cardiac
tissue,
either
directly
through
cellular
replacement
indirectly
local
paracrine
effects.
Different
types
have
been
employed
studies
infarcted
myocardium,
both
animal
models
myocardial
infarction
(MI)
well
clinical
MI
patients,
including
embryonic
cells
(ESCs)
induced
pluripotent
(iPSCs),
Muse
cells,
multipotent
such
bone
marrow-derived
mesenchymal
(MSCs)
progenitor
(CSC/CPCs).
These
delivered
is,
form
used
to
generate
tissue-engineered
(TE)
constructs
variable
results.
In
this
text,
we
sought
perform
narrative
review
experimental
employing
myocardium
within
last
two
decades,
an
emphasis
on
therapies
administered
thoracic
incision
percutaneous
coronary
interventions
(PCI),
elucidate
possible
mechanisms
action
therapeutic
effects
when
manner.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(11), P. 6211 - 6211
Published: June 5, 2024
Myocardial
infarction
activates
an
intense
fibro-inflammatory
reaction
that
is
essential
for
cardiac
remodeling
and
heart
failure
(HF).
Bioactive
peptide
galanin
plays
a
critical
role
in
regulating
cardiovascular
homeostasis;
however,
its
specific
functional
relevance
post-infarction
reprogramming
remains
obscure.
Here,
we
show
coordinates
the
trajectory
mitochondrial
integrity
reperfusion
injury.
Aberrant
deposition
of
collagen
was
associated
with
marked
increase
CD68-positive
macrophage
infiltration
tissue
mice
subjected
to
myocardial
ischemia/reperfusion
(I/R)
14
days
compared
sham
controls.
Furthermore,
found
expression
level
marker
M2
macrophages,
CD206,
significantly
down-regulated
I/R-challenged
mice.
In
contrast,
treatment
started
during
phase
blunted
responses
promoted
CD206
I/R-remodeled
hearts.
addition,
anti-apoptotic
anti-hypertrophic
effects
were
preservation
promotion
biogenesis.
These
findings
depict
as
key
arbitrator
I/R
injury
offer
promising
therapeutic
post-infarct
complications.
Cell Proliferation,
Journal Year:
2024,
Volume and Issue:
57(12)
Published: Aug. 1, 2024
Ischemic
heart
disease
(IHD)
is
a
prevalent
cardiovascular
condition
that
remains
the
primary
cause
of
death
due
to
its
adverse
ventricular
remodelling
and
pathological
changes
in
end-stage
failure.
As
complex
pathologic
condition,
it
involves
intricate
regulatory
processes
at
cellular
molecular
levels.
The
immune
system
are
closely
interconnected,
with
cells
playing
crucial
role
maintaining
cardiac
health
influencing
progression.
Consequently,
alterations
microenvironment
influenced
controlled
by
various
cells,
such
as
macrophages,
neutrophils,
dendritic
eosinophils,
T-lymphocytes,
along
cytokines
they
produce.
Furthermore,
studies
have
revealed
Gata6
