Frontiers in Cell and Developmental Biology,
Год журнала:
2024,
Номер
12
Опубликована: Сен. 3, 2024
Background
Cardiac
lipid
metabolism
reprogramming
is
recognized
as
a
critical
pathological
factor
in
the
progression
of
chronic
heart
failure
(CHF).
The
therapeutic
potential
digilanid
C
and
electroacupuncture
stimulation
(ES)
enhancing
cardiac
function
has
been
established.
However,
optimal
synergistic
regulatory
strategies
these
interventions
on
have
yet
to
be
elucidated.
Methods
This
study
aimed
comprehensively
evaluate
impact
C-ES
combination
steatosis
remodeling
CHF.
Assessments
were
conducted
across
various
dimensions,
including
myocardial
oxygen
consumption,
mitochondrial
function,
metabolism.
Additionally,
we
sought
uncover
underlying
neuromolecular
mechanisms.
Results
Our
findings,
at
both
molecular
morphological
levels,
indicated
that
application
ES
significantly
inhibited
fibrosis
steatosis.
therapy
facilitated
repair
neuro-vascular
uncoupling
induced
Notably,
ameliorated
cardiomyocyte
apoptosis
enhanced
biogenesis
CHF,
leading
restructured
energy
supply
pattern.
immunofluorescence
analyses
revealed
aggregation
glial
cells
(CGCs)
sites
abnormal
neurovascular
coupling,
response
degeneration.
was
accompanied
by
marked
reduction
abnormally
elevated
expression
interleukin
6
(IL-6)
glutamatergic
signaling,
which
correlated
with
severity
aberrant
activation
CGCs.
combined
found
activate
Janus
kinase
1
(JAK1)/signal
transducer
activator
transcription
3
(STAT3)
pathway,
effectively
attenuated
accumulation
over-recruitment
CGCs
deprivation
nerves.
Conclusion
These
findings
underscore
novel
approach
modulate
complex
interplay
between
dynamics
metabolic
dysregulation
Nature,
Год журнала:
2023,
Номер
619(7971), С. 801 - 810
Опубликована: Июль 12, 2023
The
function
of
a
cell
is
defined
by
its
intrinsic
characteristics
and
niche:
the
tissue
microenvironment
in
which
it
dwells.
Here
we
combine
single-cell
spatial
transcriptomics
data
to
discover
cellular
niches
within
eight
regions
human
heart.
We
map
cells
microanatomical
locations
integrate
knowledge-based
unsupervised
structural
annotations.
also
profile
cardiac
conduction
system
Circulation Research,
Год журнала:
2024,
Номер
134(12), С. 1681 - 1702
Опубликована: Июнь 6, 2024
Throughout
our
lifetime,
each
beat
of
the
heart
requires
coordinated
action
multiple
cardiac
cell
types.
Understanding
biology,
its
intricate
microenvironments,
and
mechanisms
that
govern
their
function
in
health
disease
are
crucial
to
designing
novel
therapeutical
behavioral
interventions.
Recent
advances
single-cell
spatial
omics
technologies
have
significantly
propelled
this
understanding,
offering
insights
into
cellular
diversity
complex
interactions
tissue.
This
review
provides
a
comprehensive
overview
landscape
heart,
bridging
gap
between
suspension-based
emerging
situ
approaches,
focusing
on
experimental
computational
challenges,
comparative
analyses
mouse
human
systems,
rising
contextualization
cells
within
niches.
As
we
explore
at
unprecedented
resolution,
integrating
from
both
studies
will
pave
way
for
diagnostic
tools
therapeutic
interventions,
ultimately
improving
outcomes
patients
with
cardiovascular
diseases.
JACC. Clinical electrophysiology,
Год журнала:
2022,
Номер
8(10), С. 1191 - 1215
Опубликована: Сен. 28, 2022
The
sinoatrial
node
(SAN)
of
the
heart
produces
rhythmic
action
potentials,
generated
via
calcium
signaling
within
and
among
pacemaker
cells.
Our
previous
work
has
described
SAN
as
composed
a
hyperpolarization-activated
cyclic
nucleotide-gated
potassium
channel
4
(HCN4)-expressing
cell
meshwork,
which
merges
with
network
connexin
43+/F-actin+
It
is
also
known
that
sympathetic
parasympathetic
innervation
create
an
autonomic
plexus
in
modulates
rate
rhythm.
However,
anatomical
details
interaction
this
meshwork
have
yet
to
be
described.
This
study
sought
describe
3-dimensional
cytoarchitecture
mouse
SAN,
including
innervation,
peripheral
glial
cells,
whole-mount
preparations
was
examined
by
three-dimensional
confocal
laser-scanning
microscopy
triple
immunolabeled
combinations
antibodies
for
HCN4,
S100
calcium-binding
protein
B
(S100B),
fibrillary
acidic
(GFAP),
choline
acetyltransferase,
or
vesicular
acetylcholine
transporter,
tyrosine
hydroxylase,
transmission
electron
microscopy.
exhibited
heterogeneous
accompanied
web
cells
novel
S100B+/GFAP–
interstitial
population,
unique
morphology
distinct
distribution
pattern,
creating
complex
interactions
other
types
node,
particularly
HCN4-expressing
Transmission
identified
similar
population
telocytes,
appeared
secrete
vesicles
toward
Application
S100B
desynchronized
Ca2+
increased
variability
impulse
plexus,
web,
type
embedded
HCN4+
increase
structural
functional
complexity
provide
new
regulatory
pathway
rhythmogenesis.
Philosophical Transactions of the Royal Society B Biological Sciences,
Год журнала:
2023,
Номер
378(1879)
Опубликована: Май 1, 2023
Even
before
the
sinoatrial
node
(SAN)
was
discovered,
cardiovascular
science
engaged
in
an
active
investigation
of
when
and
why
heart
would
beat.
After
electrochemical
theory
bioelectric
membrane
potentials
formulated
first
action
were
measured
contracting
muscle
cells,
field
became
divided:
some
investigators
studied
electrophysiology
ion
channels,
others
contraction.
It
later
known
that
changes
intracellular
Ca
2+
cause
The
pacemaking
reunited
by
coupled-clock
pacemaker
cell
function,
which
integrated
cycling
transmembrane
voltage
into
one
rhythmogenic
system.
In
this
review,
we
will
discuss
recent
discoveries
contextualize
system,
described
isolated
SAN
complex
world
tissue:
heterogeneous
local
releases,
generated
within
cells
regulated
other
types
cytoarchitecture,
variably
co-localize
synchronize
to
give
rise
relatively
rhythmic
impulses
emanate
from
excite
heart.
We
ultimately
conceptualize
as
a
brain-like
structure,
composed
intercommunicating
meshworks
multiple
interstitial
intertwined
networks
nerves
glial
more.
This
article
is
part
theme
issue
‘The
heartbeat:
its
molecular
basis
physiological
mechanisms’.
Frontiers in Cardiovascular Medicine,
Год журнала:
2022,
Номер
9
Опубликована: Авг. 4, 2022
The
ANK2
gene
encodes
for
ankyrin-B
(ANKB),
one
of
3
members
the
ankyrin
family
proteins,
whose
name
is
derived
from
Greek
word
anchor.
ANKB
was
originally
identified
in
brain
(B
denotes
“brain”)
but
has
become
most
widely
known
its
role
cardiomyocytes
as
a
scaffolding
protein
ion
channels
and
transporters,
well
an
interacting
structural
signaling
proteins.
Certain
loss-of-function
variants
are
associated
with
primarily
cardiac-presenting
autosomal-dominant
condition
incomplete
penetrance
variable
expressivity
characterized
by
predisposition
to
supraventricular
ventricular
arrhythmias,
arrhythmogenic
cardiomyopathy,
congenital
adult-onset
heart
disease,
sudden
death.
Another
independent
group
increased
risk
distinct
neurological
phenotypes,
including
epilepsy
autism
spectrum
disorders.
mechanisms
underlying
ANKB's
roles
cells
health
disease
not
fully
understood;
however,
several
clues
range
molecular
cell
biological
studies
have
emerged.
Notably,
exhibits
isoforms
that
different
cell-type–,
tissue–,
developmental
stage–
expression
profiles.
Given
conservation
within
ankyrins
across
evolution,
model
organism
enabled
discovery
could
shed
important
light
on
protein-protein
interactions
related
regulation
cellular
polarity,
organization,
calcium
homeostasis,
glucose
fat
metabolism.
Along
this
accumulation
evidence
suggesting
diversity
functions,
there
on-going
debate
disease.
We
currently
limited
understanding
how
these
functions
link
risk.
To
end,
review
will
examine
potential
contribution
functional
presentation.
This
highlight
impact
dysfunction
cardiac
neuronal
significance
AJP Heart and Circulatory Physiology,
Год журнала:
2023,
Номер
324(4), С. H373 - H390
Опубликована: Янв. 20, 2023
Growing
evidence
indicates
that
the
pathophysiological
link
between
brain
and
heart
underlies
cardiovascular
diseases,
specifically
acute
myocardial
infarction
(AMI).
Astrocytes
are
most
abundant
glial
cells
in
central
nervous
system
provide
support/protection
for
neurons.
peripheral
emerging
as
key
modulators
of
brain-heart
axis
AMI,
by
affecting
sympathetic
activity
(centrally
peripherally).
This
review,
therefore,
aimed
to
gain
an
improved
understanding
cell
AMI
risk.
includes
discussions
on
potential
role
contributing
factors
risk,
i.e.,
autonomic
dysfunction,
glial-neurotrophic
ischemic
risk
markers
[glial
line-derived
neurotrophic
factor
(GDNF),
astrocytic
S100
calcium-binding
protein
B
(S100B),
silent
ischemia,
cardiac
troponin
T
(cTnT)].
Consideration
related
certain
disorders,
namely,
blood-brain
barrier
chronic
psychological
stress,
may
improve
our
regarding
pathological
dysfunction
can
play
development/onset
AMI.
Here,
findings
demonstrated
perturbations
(especially
activity).
Moreover,
included
sympathovagal
imbalance,
low
GDNF
levels
reflecting
prothrombic
hypertension,
increased
ischemia
due
perfusion
deficits
(indicated
S100B
cTnT
levels).
Such
impacted
blood-barrier
function
were
exacerbated
during
stress.
Thus,
greater
insights
consideration
such
biomarkers
help
drive
future
studies
investigating
pathologies
a
deeper
contributions
unlock
novel
therapies
PLoS Biology,
Год журнала:
2024,
Номер
22(10), С. e3002819 - e3002819
Опубликована: Окт. 30, 2024
The
overproduction
of
cells
and
subsequent
production
debris
is
a
universal
principle
neurodevelopment.
Here,
we
show
an
additional
feature
the
developing
nervous
system
that
causes
neural
debris—promoted
by
sacrificial
nature
embryonic
microglia
irreversibly
become
phagocytic
after
clearing
other
debris.
Described
as
long-lived,
colonize
brain
persist
into
adulthood.
Using
transgenic
zebrafish
to
investigate
during
construction,
identified
unlike
cell
types
die
in
developmental
stages
they
have
expanded,
necroptosis-dependent
microglial
prevalent
when
are
expanding
brain.
Time-lapse
imaging
demonstrates
this
cannibalized
microglia.
To
features
promote
death
cannibalism,
used
time-lapse
fate-mapping
strategies
track
lifespan
individual
These
approaches
revealed
instead
being
long-lived
completely
digest
their
debris,
once
most
eventually
die,
including
ones
cannibalistic.
results
establish
paradox—which
tested
increasing
manipulating
phagocytosis—that
embryo
phagocytic,
create
then
microglia,
resulting
more
destined
die.