The Journal of Physiology,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Sept. 27, 2024
Abstract
In
our
original
white
paper
published
in
the
The
Journal
of
Physiology
2016,
we
set
out
knowledge
structural
and
functional
organization
cardiac
autonomic
control,
how
it
remodels
during
disease,
approaches
to
exploit
such
for
regulation
therapy.
aim
this
update
is
build
on
blueprint,
highlighting
significant
progress
which
has
been
made
field
since
major
challenges
opportunities
that
exist
with
regard
translation.
Imbalances
responses,
while
beneficial
short
term,
ultimately
contribute
evolution
pathology.
As
understanding
emerges
where
target
terms
actuators
(including
heart
intracardiac
nervous
system
(ICNS),
stellate
ganglia,
dorsal
root
ganglia
(DRG),
vagus
nerve,
brainstem,
even
higher
centres),
there
also
a
need
develop
sensor
technology
respond
appropriate
biomarkers
(electrophysiological,
mechanical,
molecular)
closed‐loop
therapies
can
evolve.
goal
work
endogenous
control
systems,
rather
than
opposition
them,
improve
outcomes.
image
Nature Cardiovascular Research,
Journal Year:
2022,
Volume and Issue:
1(7), P. 649 - 664
Published: July 11, 2022
Abstract
Sudden
cardiac
death,
arising
from
abnormal
electrical
conduction,
occurs
frequently
in
patients
with
coronary
heart
disease.
Myocardial
ischemia
simultaneously
induces
arrhythmia
and
massive
myocardial
leukocyte
changes.
In
this
study,
we
optimized
a
mouse
model
which
hypokalemia
combined
infarction
triggered
spontaneous
ventricular
tachycardia
ambulatory
mice,
showed
that
major
subsets
have
opposing
effects
on
conduction.
Neutrophils
increased
via
lipocalin-2
whereas
neutrophilia
associated
patients.
contrast,
macrophages
protected
against
arrhythmia.
Depleting
recruited
Ccr2
−/−
mice
or
all
macrophage
Csf1
receptor
inhibition
both
fibrillation.
Higher
burden
mortality
Cd36
Mertk
viewed
together
reduced
mitochondrial
integrity
accelerated
cardiomyocyte
death
the
absence
of
macrophages,
indicated
receptor-mediated
phagocytosis
protects
lethal
storm.
Thus,
modulation
function
provides
potential
therapeutic
pathway
for
reducing
risk
sudden
death.
Journal of Clinical Medicine,
Journal Year:
2022,
Volume and Issue:
11(15), P. 4405 - 4405
Published: July 28, 2022
Endothelial
dysfunction
is
one
of
the
earliest
manifestations
atherosclerosis,
contributing
to
its
development
and
progression.
Mental
stress
induces
endothelial
through
increased
activity
sympathetic
nervous
system,
release
corticotropin-releasing
hormone
from
hypothalamus,
inhibition
nitric
oxide
(NO)
synthesis
by
cortisol,
levels
pro-inflammatory
cytokines.
Mental-stress-induced
output
system
concomitant
withdrawal
parasympathetic
inflammatory
reflex
results
in
systemic
inflammation
activation
a
neural–hematopoietic–arterial
axis.
This
includes
brainstem
subcortical
regions
network,
bone
marrow
activation,
leukocytes
into
circulation
their
migration
arterial
wall
atherosclerotic
plaques.
Low-grade,
sterile
involved
all
steps
atherogenesis,
coronary
plaque
formation
destabilisation
rupture.
Increased
tone
may
cause
smooth-muscle-cell
proliferation,
resulting
vascular
hypertrophy,
thus
hypertension.
Emotional
events
also
instability
cardiac
repolarisation
due
brain
lateralised
imbalance
autonomic
stimulation,
which
lead
asymmetric
arrhythmia.
Acute
emotional
can
provoke
severe
catecholamine
release,
leading
direct
myocyte
injury
calcium
overload,
known
as
myocytolysis,
microvascular
vasoconstriction,
an
increase
left
ventricular
afterload.
These
changes
trigger
heart
failure
syndrome
mimicking
acute
myocardial
infarction,
characterised
transient
apical
ballooning,
(Takotsubo)
cardiomyopathy.
Women
are
more
prone
than
men
develop
mental-stress-induced
ischemia
(MSIMI),
probably
reflecting
gender
differences
patterns
during
mental
stress.
Although
guidelines
on
CV
prevention
recognise
psychosocial
factors
risk
modifiers
improve
prediction
decision
making,
evidence
that
assessment
treatment
will
prevent
CAD
needs
further
evaluation.
Signal Transduction and Targeted Therapy,
Journal Year:
2023,
Volume and Issue:
8(1)
Published: Oct. 27, 2023
Abstract
Cardiovascular
disease
(CVD)
is
the
leading
cause
of
death
in
world,
with
a
high
incidence
and
youth-oriented
tendency.
RNA
modification
ubiquitous
indispensable
cell,
maintaining
cell
homeostasis
function
by
dynamically
regulating
gene
expression.
Accumulating
evidence
has
revealed
role
aberrant
expression
CVD
caused
dysregulated
modification.
In
this
review,
we
focus
on
nine
common
modifications:
N
6
-methyladenosine
(m
A),
1
5-methylcytosine
5
C),
7
-methylguanosine
G),
4
-acetylcytosine
(ac
pseudouridine
(Ψ),
uridylation,
adenosine-to-inosine
(A-to-I)
editing,
modifications
U34
tRNA
wobble.
We
summarize
key
regulators
their
effects
expression,
such
as
splicing,
maturation,
transport,
stability,
translation.
Then,
based
classification
CVD,
mechanisms
which
occurs
progresses
through
are
discussed.
Potential
therapeutic
strategies,
therapy,
reviewed
these
mechanisms.
Herein,
some
(such
stroke
peripheral
vascular
disease)
not
included
due
to
limited
availability
literature.
Finally,
prospective
applications
challenges
discussed
for
purpose
facilitating
clinical
Moreover,
look
forward
more
studies
exploring
roles
future,
there
substantial
uncultivated
areas
be
explored.
Advanced Materials,
Journal Year:
2023,
Volume and Issue:
unknown
Published: Aug. 3, 2023
The
engineering
of
aggregation-induced
emission
luminogens
(AIEgen)
based
covalent
organic
frameworks
(COFs),
TDTA-COF,
BTDTA-COF,
and
BTDBETA-COF
are
reported,
as
hyperthermia
agents
for
inhibiting
the
occurrence
malignant
ventricular
arrhythmias
(VAs).
These
AIE
COFs
exhibit
dual
functionality,
they
not
only
directly
modulate
function
neural
activity
stellate
ganglion
(SG)
through
local
therapy
(LHT)
but
also
induce
browning
white
fat
improve
neuroinflammation
peri-SG
microenvironment,
which
is
favorable
ischemia-induced
VAs.
In
vivo
studies
have
confirmed
that
BTDBETA-COF-mediated
LHT
enhances
thermogenesis
browning-related
gene
expression,
thereby
serving
a
synergistic
role
in
combating
Transcriptome
analysis
adipose
tissue
reveals
substantial
downregulation
inflammatory
cytokines,
highlighting
potency
ameliorating
microenvironment
offering
myocardial
arrhythmia
protection.
work
on
COF-based
agent
VAs
inhibition
provides
new
avenue
mitigating
cardiac
sympathetic
nerve
hyperactivity.
The Journal of Physiology,
Journal Year:
2024,
Volume and Issue:
unknown
Published: May 22, 2024
Abstract
This
paper
updates
and
builds
on
a
previous
White
Paper
in
this
journal
that
some
of
us
contributed
to
concerning
the
molecular
cellular
basis
cardiac
neurobiology
heart
disease.
Here
we
focus
recent
findings
underpin
autonomic
development,
novel
intracellular
pathways
neuroplasticity.
Throughout
highlight
unanswered
questions
areas
controversy.
Whilst
neurochemical
are
already
demonstrating
prognostic
viability
patients
with
failure,
also
discuss
opportunity
better
understand
sympathetic
impairment
by
using
patient
specific
stem
cells
provides
pathophysiological
contextualization
study
‘disease
dish’.
Novel
imaging
techniques
spatial
transcriptomics
facilitating
road
map
for
target
discovery
may
form
therapeutic
treat
dysautonomia.
image
Journal of Nuclear Cardiology,
Journal Year:
2025,
Volume and Issue:
unknown, P. 102146 - 102146
Published: Feb. 1, 2025
Cardiac
sympathetic
neuronal
dysfunction
is
an
early
marker
in
wild-type
transthyretin
amyloidosis
cardiomyopathy
(ATTRwt-CM).
[123I]-MIBG
imaging
evaluates
cardiac
innervation
but
lacks
volumetric
activity
quantification
current
methods.
This
study
aims
to
quantify
ATTRwt-CM
using
SPECT/CT
and
correlate
findings
with
functional
structural
parameters
from
echocardiogram
magnetic
resonance
(CMR).
We
conducted
a
single-center,
descriptive,
cross-sectional
absolute
myocardial
function
SPECT/CT.
Retrospective
reconstruction
allowed
for
tracer-uptake
of
the
left
ventricle,
overall
segmented,
kBq/mL,
SUV
percentage
injected
dose
(%ID).
Echocardiography,
CMR,
bone
scintigraphy
were
performed
according
clinical
standards.
Segmented
values
correlated
global
longitudinal
strain
(GLSS)
on
echocardiography,
native-T1,
extracellular
volume
(ECV)
CMR
fused
CMR.
Twenty-nine
patients
(75.8±6.6
years,
90%
male)
prospectively
included.
All
exhibited
dysfunction,
median
late
heart-to-mediastinum
ratio
1.69[1.45-1.89]
washout
rate
22.7%
(16.4-27.3%).
SUVmean,
SUVpeak,
SUVmax
%ID
1.80
±
0.78,
3.84
1.41,
4.46
1.68
0.46
0.18
respectively,
correlating
semi-quantitative
measures.
No
correlations
found
GLSS
echocardiography
or
native
T1
ECV
The
demonstrates
feasibility
ATTRwt-CM.
measures
not
key
confirms
sensitivity
different
aspects
pathology.
EudraCT
ref.
2020-003350-72,
retrospectively
registered
20
March
2023.
https://classic.
gov/ct2/show/NCT05776212.
Circulation Research,
Journal Year:
2025,
Volume and Issue:
136(6), P. 618 - 627
Published: March 13, 2025
Neurocardiology
is
an
interdisciplinary
field
that
examines
the
complex
interactions
between
nervous
and
cardiovascular
systems,
exploring
how
neurological
processes,
such
as
autonomic
system
regulation
brain-heart
communication
impact
heart
function
contribute
to
health
disease.
Although
much
of
focus
on
has
centered
traditional
risk
factors,
influence
system,
especially
in
females,
increasingly
recognized
a
key
determinant
outcomes.
This
article
reviews
existing
literature
mechanisms
females.
Specifically,
we
analyze
primary
disorders
including
cerebrovascular
disease,
headache
disorders,
multiple
sclerosis
have
specific
downstream
effects
cardiac
function.
By
understanding
relationship
health,
this
review
highlights
need
for
sex-specific
approaches
prevention,
diagnosis,
treatment
disease
ultimately
encouraging
discovery
more
effective
care
strategies
improving
Frontiers in Physiology,
Journal Year:
2021,
Volume and Issue:
12
Published: Sept. 9, 2021
In
cardiomyocytes,
invaginations
of
the
sarcolemmal
membrane
called
t-tubules
are
critically
important
for
triggering
contraction
by
excitation-contraction
(EC)
coupling.
These
structures
form
functional
junctions
with
sarcoplasmic
reticulum
(SR),
and
thereby
enable
close
contact
between
L-type
Ca
2+
channels
(LTCCs)
Ryanodine
Receptors
(RyRs).
This
arrangement
in
turn
ensures
efficient
release,
contraction.
While
new
data
indicate
that
capable
exhibiting
compensatory
remodeling,
they
also
widely
reported
to
be
structurally
functionally
compromised
during
disease,
resulting
disrupted
homeostasis,
impaired
systolic
and/or
diastolic
function,
arrhythmogenesis.
review
summarizes
these
findings,
while
highlighting
an
emerging
appreciation
distinct
roles
pathophysiology
heart
failure
reduced
preserved
ejection
fraction
(HFrEF
HFpEF).
this
context,
we
current
understanding
processes
underlying
t-tubule
growth,
maintenance,
degradation,
underscoring
involvement
a
variety
regulatory
proteins,
including
junctophilin-2
(JPH2),
amphiphysin-2
(BIN1),
caveolin-3
(Cav3),
newer
candidate
proteins.
Upstream
regulation
structure/function
cardiac
workload
specifically
ventricular
wall
stress
is
discussed,
alongside
perspectives
novel
strategies
which
may
therapeutically
target
mechanisms.