Pharmacological Research,
Journal Year:
2024,
Volume and Issue:
unknown, P. 107539 - 107539
Published: Dec. 1, 2024
Long
non-coding
RNAs
(lncRNAs)
have
emerged
as
pivotal
regulators
of
cancer
pathogenesis,
influencing
various
cellular
processes
and
contributing
to
tumorigenesis.
Sphingolipid
metabolism
has
garnered
interest
a
potential
target
for
therapy
owing
its
considerable
diagnostic
prognostic
value.
Recent
studies
demonstrated
that
lncRNAs
regulate
tumor-associated
metabolic
reprogramming
via
sphingolipid
metabolism.
However,
the
precise
nature
interactions
between
remains
unclear.
This
review
summarizes
key
roles
in
We
emphasize
interaction
influences
their
impact
on
both
prognosis
drug
resistance.
These
findings
suggest
lncRNA-sphingolipid
holds
great
newl
treatment.
Journal of Cardiovascular Development and Disease,
Journal Year:
2025,
Volume and Issue:
12(3), P. 83 - 83
Published: Feb. 22, 2025
While
the
heart
works
as
an
efficient
pump,
it
also
has
a
high
level
of
adaptivity
by
changing
its
structure
to
maintain
function
during
healthy
and
diseased
states.
In
this
Review,
we
present
examples
structure–function
relationships
across
species
throughout
embryonic
development
in
mammals
birds.
We
summarize
current
research
on
avian
models
aiming
at
understanding
how
biophysical
biological
mechanisms
closely
interact
formation.
conclude
underscoring
similarities
between
cardiac
adaptations
structural
changes
over
developmental
evolutionary
time
scales
behind
these
can
help
prevent
or
alleviate
effects
malformations
contribute
regeneration
efforts.
Heart,
Journal Year:
2025,
Volume and Issue:
unknown, P. heartjnl - 325442
Published: March 4, 2025
Following
injury,
many
organs
are
capable
of
rapid
regeneration
necrotic
tissue
to
regain
normal
function.
In
contrast,
the
damaged
heart
typically
replaces
with
a
collagen-rich
scar,
due
limited
regenerative
capacity
its
functional
contractile
cardiomyocytes
(CMs).
However,
this
varies
dramatically
during
development
and
between
species.
Furthermore,
studies
have
shown
that
cardiac
can
be
enhanced
return
function
following
myocardial
infarction
(MI).
review,
we
outline
proliferative
CMs
in
utero,
postnatally
adulthood.
We
also
describe
MI
injury.
Finally,
focus
on
various
therapeutic
strategies
aim
augment
preclinical
animal
models.
These
include
altering
transcripts,
microRNAs,
extracellular
matrix
proteins
inducing
metabolic
rewiring.
Together,
these
therapies
potentially
improve
lives
millions
failure
patients
currently
suffering
worldwide.
Frontiers in Cardiovascular Medicine,
Journal Year:
2025,
Volume and Issue:
12
Published: April 28, 2025
The
limited
capacity
of
adult
mammalian
cardiomyocytes
to
undergo
cell
division
and
proliferation
is
one
the
key
factors
contributing
heart
failure.
In
newborn
mice,
cardiac
occurs
during
a
brief
window,
but
this
proliferative
diminishes
by
7
days
after
birth.
Current
studies
on
regeneration
focused
elucidating
changes
in
regulatory
within
before
aiming
determine
whether
potential
association
between
these
cycle
arrest
cardiomyocytes.
Facilitating
re-entry
into
or
reversing
their
exit
from
it
represents
critical
strategy
for
regeneration.
This
paper
provides
an
overview
role
regeneration,
briefly
describes
cardiomyocyte
systematically
summarizes
regulation
cardiomyocytes,
metabolic
mechanisms
underlying
arrest.
Additionally,
we
highlight
development
cardiovascular
disease
drugs
targeting
status
clinical
treatment.
Our
goal
outline
strategies
promoting
repair
following
injury,
while
also
pointing
toward
future
research
directions
that
may
offer
new
technologies
prospects
treating
diseases,
such
as
myocardial
infarction,
arrhythmia
FEBS Letters,
Journal Year:
2024,
Volume and Issue:
598(21), P. 2641 - 2655
Published: July 4, 2024
Cardiometabolic
disorders
contribute
to
the
global
burden
of
cardiovascular
diseases.
Emerging
sphingolipid
metabolites
like
sphingosine‐1‐phosphate
(S1P)
and
its
receptors,
S1PRs,
present
a
dynamic
signalling
axis
significantly
impacting
cardiac
homeostasis.
S1P's
intricate
mechanisms
extend
transportation
in
bloodstream
by
two
specific
carriers:
high‐density
lipoprotein
particles
albumin.
This
transport
system
ensures
accessibility
S1P
distant
target
tissues,
influencing
several
physiological
processes
critical
for
health.
review
delves
into
diverse
functions
S1PRs
both
pathophysiological
conditions
heart.
Emphasis
is
placed
on
their
roles
modulating
health,
spanning
from
contractility,
angiogenesis,
inflammation,
atherosclerosis
myocardial
infarction.
The
interplays
involving
receptors
are
analysed
concerning
different
cell
types,
shedding
light
respective
heart
We
also
therapeutic
applications
targeting
S1P/S1PRs
diseases,
considering
existing
drugs
Fingolimod,
as
well
prospects
challenges
developing
novel
therapies
that
selectively
modulate
S1PRs.
Journal of the American Heart Association,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Oct. 29, 2024
Background
The
proliferative
capacity
of
cardiomyocytes
in
adult
mammalian
hearts
is
far
too
low
to
replace
the
cells
that
are
lost
myocardial
infarction.
Both
cardiomyocyte
proliferation
and
regeneration
can
be
improved
via
overexpression
a
constitutively
active
variant
YAP5SA
(Yes‐associated
protein,
5SA
[active]
mutant),
but
persistent
proliferation‐inducing
genes
could
lead
hypertrophy
arrhythmia,
whereas
off‐target
expression
fibroblasts
macrophages
increase
fibrosis
inflammation.
Methods
Results
Transient
or
GFP
(green
fluorescent
protein;
control)
was
targeted
our
cardiomyocyte‐specific
modified
mRNA
translation
system
(
CM‐SMRTs
CM‐SMRTs,
respectively).
YAP5SA‐cardiomyocyte
specificity
confirmed
vitro
experiments
cardiac
had
been
differentiated
from
human
induced‐
pluripotent
stem
umbilical‐vein
endothelial
cells,
regenerative
potency
evaluated
mouse
infarction
model.
In
cultured
induced‐pluripotent
cells‐cardiomyocytes,
YAP
abundantly
expressed
for
3
days
after
administration
accompanied
by
increases
markers
proliferation,
before
declining
near‐background
levels
day
7,
fluorescence
remained
high
1
treatment
then
slowly
declined.
also
observed
cells‐cardiac
on
declined
substantially
3.
model,
echocardiographic
assessments
left‐ventricular
ejection
fraction
fractional
shortening
were
significantly
greater,
infarct
sizes
smaller
CM‐SMRTs–treated
mice
than
vehicle‐treated
control
animals,
appeared
promote
proliferation.
Conclusions
used
transiently
specifically
overexpress
cardiomyocytes,
this
strategy
promoted
Frontiers in Cell and Developmental Biology,
Journal Year:
2024,
Volume and Issue:
12
Published: July 10, 2024
The
adult
mammalian
cardiomyocyte
has
a
limited
capacity
for
self-renewal,
which
leads
to
the
irreversible
heart
dysfunction
and
poses
significant
threat
myocardial
infarction
patients.
In
past
decades,
research
efforts
have
been
predominantly
concentrated
on
proliferation
regeneration.
However,
is
complex
organ
that
comprises
not
only
cardiomyocytes
but
also
numerous
noncardiomyocyte
cells,
all
playing
integral
roles
in
maintaining
cardiac
function.
addition,
are
exposed
dynamically
changing
physical
environment
includes
oxygen
saturation
mechanical
forces.
Recently,
growing
number
of
studies
microenvironment
regeneration
ongoing.
this
review,
we
provide
an
overview
recent
advances
microenvironment,
plays
important
role
STAR Protocols,
Journal Year:
2024,
Volume and Issue:
5(3), P. 103204 - 103204
Published: July 21, 2024
Here,
we
present
a
protocol
for
the
quantitative
assessment
of
rat
and
mouse
cardiomyocyte
proliferation
both
in
vitro
vivo.
For
vivo
approach,
describe
steps
isolation
neonatal
cardiomyocytes
employment
various
indicators
to
quantify
cell
proliferation.
We
then
detail
procedures
that
incorporate
comprehensive
assays
genetic
lineage
tracing
strategy
evaluate
endogenous
This
can
be
modified
investigate
other
mammalian
complete
details
on
use
execution
this
protocol,
please
refer
Ji
et
al.