In
response
to
various
stressors,
cardiac
chambers
undergo
structural
remodeling.
Long-term
exposure
of
the
right
ventricle
(RV)
pressure
or
volume
overload
leads
its
maladaptive
remodeling,
associated
with
RV
failure
and
increased
mortality.
While
left
ventricular
adverse
remodeling
is
well
understood
therapeutic
options
are
available
emerging,
remains
underexplored
no
specific
therapies
currently
available.
Accumulating
evidence
implicates
a
role
mast
cells
in
Mast
produce
release
numerous
inflammatory
mediators,
growth
factors
proteases
that
can
adversely
affect
cells,
thus
contributing
Recent
experimental
findings
suggest
might
represent
potential
target.
This
review
examines
focus
on
explores
efficacy
interventions
targeting
mitigate
Arteriosclerosis Thrombosis and Vascular Biology,
Год журнала:
2024,
Номер
44(3), С. 690 - 697
Опубликована: Янв. 25, 2024
BACKGROUND:
Clonal
hematopoiesis
of
indeterminate
potential
(CHIP)
is
an
acquired
genetic
risk
factor
for
both
leukemia
and
cardiovascular
disease.
It
results
in
proinflammatory
myeloid
cells
the
bone
marrow
blood;
however,
how
these
behave
tissue
remains
unclear.
Our
study
aimed
at
investigating
whether
CHIP-mutated
macrophages
accumulate
preferentially
tissues
examining
transcriptome
from
DNMT3A
(DNA
methyltransferase
3
alpha)
or
TET2
(Tet
methylcytosine
dioxygenase
2)
mutation
carriers.
METHODS:
We
recruited
patients
undergoing
carotid
endarterectomy
heart
surgeries
to
screen
CHIP
carriers
using
targeted
genomic
sequencing.
Myeloid
lymphoid
were
isolated
blood
collected
during
flow
cytometry.
DNA
RNA
extracted
sorted
subjected
variant
allele
frequency
measurement
droplet
digital
polymerase
chain
reaction
transcriptomic
profiling
bulk
sequencing,
respectively.
RESULTS:
Using
reaction,
we
detected
similar
monocytes
atheromas
tissues,
even
among
with
without
CCR2
(C-C
motif
chemokine
receptor
expression.
Bulk
sequencing
revealed
a
gene
profile
compared
those
noncarriers.
CONCLUSIONS:
Quantitatively,
did
not
but
qualitatively,
they
expressed
more
disease-prone
phenotype.
Frontiers in Cardiovascular Medicine,
Год журнала:
2024,
Номер
11
Опубликована: Июль 11, 2024
Cardiotoxicity
can
be
defined
as
“chemically
induced
heart
disease”,
which
occur
with
many
different
drug
classes
treating
a
range
of
diseases.
It
is
the
primary
cause
attrition
during
pre-clinical
development
and
withdrawal
from
market.
Drug
cardiovascular
toxicity
result
both
functional
effects
alteration
contractile
electrical
regulation
in
structural
changes
morphological
to
cardiomyocytes
other
cardiac
cells.
These
adverse
conditions
such
arrhythmia
or
more
serious
reduction
left
ventricular
ejection
fraction
(LVEF),
lead
failure
death.
Anticancer
drugs
adversely
affect
cardiomyocyte
function
well
fibroblasts
endothelial
cells,
interfering
autocrine
paracrine
signalling
between
these
cell
types
ultimately
altering
cellular
homeostasis.
This
review
aims
highlight
potential
mechanisms
involving
non-cardiomyocyte
cells
by
first
introducing
physiological
roles
within
myocardium
secondly,
identifying
pathways
perturbed
anticancer
Abstract
Glycoproteins,
representing
a
significant
proportion
of
posttranslational
products,
play
pivotal
roles
in
various
biological
processes,
such
as
signal
transduction
and
immune
response.
Abnormal
glycosylation
may
lead
to
structural
functional
changes
glycoprotein,
which
is
closely
related
the
occurrence
development
diseases.
Consequently,
exploring
protein
can
shed
light
on
mechanisms
behind
disease
manifestation
pave
way
for
innovative
diagnostic
therapeutic
strategies.
Nonetheless,
study
clinical
glycoproteomics
fraught
with
challenges
due
low
abundance
intricate
structures
glycosylation.
Recent
advancements
mass
spectrometry‐based
have
improved
our
ability
identify
abnormal
glycoproteins
samples.
In
this
review,
we
aim
provide
comprehensive
overview
foundational
principles
recent
glycoproteomic
methodologies
applications.
Furthermore,
discussed
typical
characteristics,
underlying
functions,
diseases,
brain
cardiovascular
cancers,
kidney
metabolic
Additionally,
highlighted
potential
avenues
future
glycoproteomics.
These
insights
provided
review
will
enhance
comprehension
methods
diseases
promote
elucidation
pathogenesis
discovery
novel
biomarkers
targets.
Journal of Cardiovascular Development and Disease,
Год журнала:
2024,
Номер
11(2), С. 54 - 54
Опубликована: Фев. 4, 2024
In
response
to
various
stressors,
cardiac
chambers
undergo
structural
remodeling.
Long-term
exposure
of
the
right
ventricle
(RV)
pressure
or
volume
overload
leads
its
maladaptive
remodeling,
associated
with
RV
failure
and
increased
mortality.
While
left
ventricular
adverse
remodeling
is
well
understood
therapeutic
options
are
available
emerging,
remains
underexplored,
no
specific
therapies
currently
available.
Accumulating
evidence
implicates
role
mast
cells
in
Mast
produce
release
numerous
inflammatory
mediators,
growth
factors
proteases
that
can
adversely
affect
cells,
thus
contributing
Recent
experimental
findings
suggest
might
represent
a
potential
target.
This
review
examines
focus
on
explores
efficacy
interventions
targeting
mitigate
Intensive Care Medicine Experimental,
Год журнала:
2024,
Номер
12(1)
Опубликована: Май 11, 2024
Abstract
Background
Catecholamines
are
commonly
used
as
therapeutic
drugs
in
intensive
care
medicine
to
maintain
sufficient
organ
perfusion
during
shock.
However,
excessive
or
sustained
adrenergic
activation
drives
detrimental
cardiac
remodeling
and
may
lead
heart
failure.
Whether
catecholamine
treatment
absence
of
failure
causes
persistent
injury,
is
uncertain.
In
this
experimental
study,
we
assessed
the
course
recovery
after
prolonged
investigated
molecular
mechanisms
involved.
Results
C57BL/6N
wild-type
mice
were
assigned
14
days
with
isoprenaline
phenylephrine
(IsoPE),
IsoPE
subsequent
recovery,
healthy
control
groups.
improved
left
ventricular
contractility
but
caused
substantial
fibrosis
hypertrophy.
discontinuation
treatment,
these
alterations
largely
reversible.
To
uncover
involved,
performed
RNA
sequencing
from
isolated
cardiomyocyte
nuclei.
resulted
a
transient
upregulation
genes
related
extracellular
matrix
formation
transforming
growth
factor
signaling.
While
components
receptor
signaling
downregulated
observed
an
endothelin-1
its
receptors
cardiomyocytes,
indicating
crosstalk
between
both
pathways.
follow
finding,
treated
endothelin-1.
Compared
IsoPE,
induced
minor
longer
lasting
changes
gene
expression.
DNA
methylation-guided
analysis
enhancer
regions
identified
immediate
early
transcription
factors
such
AP-1
family
members
Jun
Fos
key
drivers
pathological
expression
following
treatment.
Conclusions
The
results
study
show
that
exposure
induces
adverse
before
onset
dysfunction
which
has
implications
for
clinical
practice.
depend
on
type
stimulus
reversible
Crosstalk
endothelin
downstream
provide
new
opportunities
more
targeted
approaches
help
separate
desired
undesired
effects
Pharmacological Reviews,
Год журнала:
2024,
Номер
76(5), С. 846 - 895
Опубликована: Июнь 12, 2024
Cardiometabolic
diseases
(CMDs)
are
major
contributors
to
global
mortality,
emphasizing
the
critical
need
for
novel
therapeutic
interventions.
Hydrogen
sulfide
(H2S)
has
garnered
enormous
attention
as
a
significant
gasotransmitter
with
various
physiological,
pathophysiological,
and
pharmacological
impacts
within
mammalian
cardiometabolic
systems.
In
addition
its
roles
in
attenuating
oxidative
stress
inflammatory
response,
burgeoning
research
emphasizes
significance
of
H2S
regulating
proteins
via
persulfidation,
well-known
modification
intricately
associated
pathogenesis
CMDs.
This
review
seeks
investigate
recent
updates
on
physiological
actions
endogenous
donors
addressing
diverse
aspects
CMDs
across
cellular,
animal,
clinical
studies.
Of
note,
advanced
methodologies
including
multi-omics,
intestinal
microflora
analysis,
organoid
single-cell
sequencing
techniques
gaining
traction
due
their
ability
offer
comprehensive
insights
into
biomedical
research.
These
emerging
approaches
hold
promise
characterizing
health
diseases.
We
will
critically
assesse
current
literatures
clarify
while
also
delineating
opportunities
challenges
they
present
H2S-based
pharmacotherapy
Significance
Statement
The
covers
developments
biology
pharmacology
Endogenous
show
great
management
by
numerous
signaling
pathways.
emergence
new
technologies
considerably
advance
translation
H2S.
Basic Research in Cardiology,
Год журнала:
2024,
Номер
unknown
Опубликована: Окт. 15, 2024
Abstract
Chronic
kidney
disease
(CKD)
predisposes
to
cardiac
remodeling
and
coronary
microvascular
dysfunction.
Studies
in
swine
identified
changes
structure
function,
as
well
mitochondrial
oxidative
stress.
However,
CKD
was
combined
with
metabolic
derangement,
thereby
obscuring
the
contribution
of
alone.
Therefore,
we
studied
impact
on
heart
proteome
studies
measurement
function
perfusion
identify
processes
involved
CKD.
induced
at
10–12
weeks
age
while
sham-operated
served
controls.
5–6
months
later,
left
ventricular
(LV)
flow
reserve
were
measured.
LC–MS–MS-based
proteomic
analysis
LV
tissue
performed.
myocardium
kidneys
histologically
examined
for
interstitial
fibrosis
Renal
embolization
resulted
mild
chronic
injury
(increased
urinary
NGAL).
PV
loops
showed
dilation
increased
wall
stress,
preload
recruitable
stroke
work
impaired
Quantitative
STRING
pre-ranked
functional
enrichments
pathways
related
contractile
reactive
oxygen
species,
extracellular
matrix
(ECM)
remodeling,
which
confirmed
associated
total
anti-oxidant
capacity.
H
2
O
exposure
myocardial
slices
from
CKD,
but
not
normal
swine,
function.
Furthermore,
proteins
downregulated
suggesting
dysfunction
higher
basal
blood
flow.
Thus,
induces
alterations
along
proteins,
stress
ECM
that
perfusion.
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Ноя. 11, 2024
Summary
The
heart
is
one
of
the
least
regenerative
organs
in
humans,
and
ischemic
disease
leading
cause
death
worldwide.
Understanding
cellular
molecular
processes
that
occur
during
cardiac
wound
healing
an
essential
prerequisite
to
reducing
health
burden
improve
function
after
myocardial
tissue
damage.
By
integrating
single-cell
RNA-sequencing
with
imaging-based
spatial
transcriptomics,
we
reconstructed
spatio-temporal
dynamics
fibrotic
niche
ventricular
injury
adult
mice.
Our
analysis
reveals
dynamic
regulation
local
cell
communication
niches
over
time.
We
identified
interactions
regulate
repair,
including
fibroblast
proliferation
silencing
by
Trem2
high
macrophages
prevents
excessive
fibrosis.
Moreover,
discovered
a
rare
population
dedifferentiating
cardiomyocytes
early
post-lesion
stages,
which
was
sustained
signals
from
myeloid
lymphoid
cells.
Culturing
non-regenerative
mouse
or
human
these
factors
reactivated
progenitor
gene
expression
cycle
activity.
In
summary,
this
type
atlas
provides
valuable
insights
into
heterocellular
control
repair.
Highlights
scRNA-seq
situ
sequencing
reveal
repair
Local
coordinate
overall
response
Fibroblast
suppresses
fibrosis
Cardiomyocyte
plasticity
promoted
cells
