Pathologia,
Год журнала:
2023,
Номер
20(1), С. 5 - 13
Опубликована: Апрель 28, 2023
Intermittent
hypoxia
has
been
studied
for
many
years
as
a
promising
non-pharmacological
method
of
cardiovascular
disease
prevention.
Hypoxic
effects
are
accompanied
by
structural
and
functional
changes
in
the
myocardium.
There
is
direct
link
between
duration
hypoxic
exposures
severity
left
ventricular
myocardial
remodeling.
A
range
histochemical
markers
remodeling
(cardiotrophin-1,
titin,
collagen
type
1,
annexin
V)
characterizing
parenchymal-stromal
relationships
myocardium
shown
high
informativeness
prognostic
value.
The
aim
study
was
to
examine
cardiotrophin-1,
V
morphofunctional
state
ventricle
heart
experimental
rats
exposed
intermittent
15-day
(IH15)
60-day
(IH60).
Materials
methods.
modeled
using
30
normotensive
male
Wistar
rats,
7–8
months
old,
which
were
randomly
assigned
3
groups
10
animals
each:
1)
INT
–
control
group
intact
(196.3
±
6.8
g);
2)
IH15
(205.6
4.1
3)
IH60
(201.1
5.5
g).
compared
varying
duration:
hypoxia.
Experimental
modeling
2
terms
revealed
number
differences
dependent
on
this
factor
through
(blood
pressure
measurement,
echocardiography)
immunofluorescent
studies.
Results.
Blood
both
range,
but
an
increase
systolic
%
diastolic
19
found
(p
<
0.05).
In
group,
there
significant
decrease
end-diastolic
dimension
20
%,
end-systolic
22
thickness
posterior
wall
44
interventricular
septum
33
well
mass
12
indicating
concentric
ventricle,
development
confirmed
76
relative
that
Along
with
these
changes,
volume
47
48
stroke
49
cardiac
output
50
preserved
ejection
fraction
While
parameters
characterized
17
23
15
higher
than
value
At
same
time,
9
decreased
24
increased
Also,
58
8
concentrations
exceeded
those
IH15,
namely:
cardiotrophin-1
39
titin
70
1
60
130
Conclusions.
forms
hypertrophy
according
echocardiography
findings;
marker
profile
moderate
resilient-elastic
properties
intensity
cardiomyocyte
death.
Remodeling
caused
eccentric
pattern
severe
hypertrophy,
fibrosis
associated
apoptosis
cardiomyocytes.
Such
may
indicate
initial
stages
maladaptation,
increasing
risk
failure
development.
Redox Biology,
Год журнала:
2024,
Номер
71, С. 103109 - 103109
Опубликована: Март 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.
Phytomedicine,
Год журнала:
2024,
Номер
127, С. 155467 - 155467
Опубликована: Фев. 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.
International Immunopharmacology,
Год журнала:
2025,
Номер
146, С. 113710 - 113710
Опубликована: Янв. 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.
Biomedicines,
Год журнала:
2025,
Номер
13(2), С. 259 - 259
Опубликована: Янв. 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.
Frontiers in Pharmacology,
Год журнала:
2025,
Номер
16
Опубликована: Март 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.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(11), С. 6211 - 6211
Опубликована: Июнь 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.
Materials Today Bio,
Год журнала:
2025,
Номер
31, С. 101476 - 101476
Опубликована: Янв. 9, 2025
Stem
cell-based
therapy
has
emerged
as
a
promising
approach
for
heart
repair,
potentially
regenerating
damaged
tissue
and
improving
outcomes
patients
with
disease.
However,
the
efficacy
of
stem
therapies
remains
limited
by
several
challenges,
including
poor
cell
survival,
low
retention
rates,
integration,
functional
outcomes.
This
article
reviews
current
enhancement
strategies
to
optimize
mesenchymal
cardiac
repair.
Key
approaches
include
optimizing
delivery
methods,
enhancing
engraftment,
promoting
functions
through
genetic
molecular
modifications,
paracrine
effects
cells,
leveraging
biomaterials
engineering
techniques.
By
focusing
on
these
techniques,
paper
highlights
innovative
that
can
transform
into
more
viable
effective
treatment
option
The
ongoing
research
technological
advancements
continue
push
boundaries,
hoping
make
mainstream
International Journal of Nanomedicine,
Год журнала:
2025,
Номер
Volume 20, С. 1747 - 1768
Опубликована: Фев. 1, 2025
Abstract:
Myocardial
infarction
(MI)
is
the
leading
cause
of
mortality
from
cardiovascular
diseases.
Rapid
diagnosis
and
effective
treatment
are
critical
for
improving
patient
prognosis.
Although
current
diagnostic
therapeutic
approaches
have
made
significant
progress,
they
still
face
challenges
such
as
ischemia-reperfusion
injury,
microcirculatory
disorders,
adverse
cardiac
remodeling,
inflammatory
responses.
These
issues
highlight
urgent
need
innovative
solutions.
Nanomaterials,
with
their
diverse
types,
excellent
physicochemical
properties,
biocompatibility,
targeting
capabilities,
offer
promising
potential
in
addressing
these
challenges.
Advances
nanotechnology
increasingly
drawn
attention
to
application
nanomaterials
both
diagnosing
treating
myocardial
infarction.
We
summarize
pathophysiological
mechanisms
staging
systematically
review
applications
MI
diagnosis,
including
detection
biomarkers
imaging
techniques,
well
treatment,
encompassing
anti-inflammatory
effects,
antioxidant
stress,
inhibition
fibrosis,
promotion
angiogenesis,
conduction
repair.
analyze
existing
provide
insights
into
future
research
directions
Specifically,
we
discuss
rigorous
safety
assessments,
long-term
efficacy
studies,
development
robust
strategies
translating
laboratory
findings
clinical
practice.
In
conclusion,
holds
promise
a
new
strategy
Its
enhance
outcomes
revolutionize
care
makes
it
an
exciting
area
practical
real-world
settings.
Keywords:
infarction,
nanomaterials,
nanoparticles,