International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
26(1), P. 231 - 231
Published: Dec. 30, 2024
Myocardial
infarction
(MI)
is
a
highly
challenging
and
fatal
disease,
with
diverse
challenges
arising
at
different
stages
of
its
progression.
As
such,
non-coding
RNAs
(ncRNAs),
which
can
broadly
regulate
cell
fate,
stem
cells
multi-differentiation
potential
are
emerging
as
novel
therapeutic
approaches
for
treating
MI
across
various
stages.
NcRNAs,
including
microRNAs
(miRNAs)
long
(LncRNAs),
directly
participate
in
regulating
intracellular
signaling
pathways,
influence
cardiac
angiogenesis,
promote
the
repair
infarcted
myocardium.
Currently,
commonly
used
medicine,
such
mesenchymal
(MSCs)
induced
pluripotent
(iPSCs),
differentiate
into
human
types
without
ethical
concerns.
When
combined
ncRNAs,
these
more
effectively
induce
directed
differentiation,
angiogenesis
heart,
replenish
normal
cells.
Additionally,
cell-derived
exosomes,
contain
improve
myocardial
damage
region
through
paracrine
mechanisms.
However,
our
understanding
specific
roles
mechanisms
cells,
exosomes
secreted
by
during
remains
limited.
Therefore,
this
review
systematically
categorizes
MI,
aiming
to
summarize
direct
regulatory
effects
ncRNAs
on
an
myocardium
points
disease
Moreover,
it
explores
therapy
exosome
complex
pathological
evolution
process.
The
objective
was
provide
insights
strategies
open
new
research
directions
application
field
repair.
Pacing and Clinical Electrophysiology,
Journal Year:
2024,
Volume and Issue:
47(3), P. 417 - 428
Published: Feb. 20, 2024
Abstract
Background
Atrial
fibrillation
(AF)
is
a
common
heart
rhythm
disorder
that
associated
with
an
increased
risk
of
stroke
and
failure
(HF).
Initially,
association
between
AF
ion
channel
dysfunction
was
identified,
classifying
the
pathology
as
predominantly
electrical
disease.
More
recently
it
has
been
recognized
fibrosis
structural
atrial
remodeling
play
driving
role
in
development
this
arrhythmia
also
these
cases.
Purpose
Understanding
genetic
determined
could
be
important
to
better
comprise
pathophysiology
refine
its
management
nongenetic
forms.
In
review
we
analyze
epigenetic
mechanisms
responsible
for
their
link
fibrosis,
then
will
consider
analogies
pathophysiological
mechanism
AF,
discuss
consequent
therapeutic
options.
Non-coding RNA Research,
Journal Year:
2024,
Volume and Issue:
9(4), P. 1222 - 1234
Published: May 20, 2024
Ferroptosis,
a
form
of
regulated
cell
death,
has
emerged
as
crucial
process
in
diverse
pathophysiological
states,
encompassing
cancer,
neurodegenerative
ailments,
and
ischemia-reperfusion
injury.
The
glutathione
(GSH)-dependent
lipid
peroxidation
pathway,
chiefly
governed
by
peroxidase
4
(GPX4),
assumes
an
essential
part
driving
ferroptosis.
GPX4,
the
principal
orchestrator
ferroptosis,
garnered
significant
attention
across
cardiovascular,
neuroscience
domains
over
past
decade.
Noteworthy
investigations
have
elucidated
indispensable
functions
ferroptosis
numerous
diseases,
including
tumorigenesis,
wherein
robust
within
cells
can
impede
tumor
advancement.
Recent
research
underscored
complex
regulatory
role
non-coding
RNAs
(ncRNAs)
regulating
GSH-GPX4
network,
thus
influencing
cellular
susceptibility
to
This
exhaustive
review
endeavors
probe
into
multifaceted
processes
which
ncRNAs
control
network
Specifically,
we
delve
miRNAs,
lncRNAs,
circRNAs
GPX4
expression
impacting
Moreover,
discuss
clinical
implications
dysregulated
interactions
between
several
conditions,
underscoring
their
capacity
viable
targets
for
therapeutic
intervention.
Additionally,
explores
emerging
strategies
aimed
at
targeting
modulate
pathway
manipulate
advantage.
A
comprehensive
understanding
these
intricate
networks
furnishes
insights
innovative
avenues
diseases
associated
with
perturbed
thereby
laying
groundwork
interventions
ferroptosis-related
pathological
conditions.
Frontiers in Cardiovascular Medicine,
Journal Year:
2025,
Volume and Issue:
12
Published: April 4, 2025
Circadian
rhythm,
or
the
biological
clock,
is
an
intrinsic
timing
system
present
in
organisms
that
operates
on
a
cycle
of
approximately
24
h.
Nearly
every
cell
human
body
adheres
to
specific
circadian
governing
various
processes
essential
for
overall
health.
REV-ERB,
key
clock-regulating
gene,
plays
crucial
role
maintaining
precision
these
rhythms.
This
gene
influences
many
downstream
targets
associated
with
diverse
pathophysiological
processes,
including
metabolism,
autophagy,
immunity,
inflammation,
and
aging
across
multiple
organs.
REV-ERB
specifically
impacts
cardiac
systolic
function
by
regulating
myocardial
energy
metabolism.
In
contemporary
society,
health
well-being
are
increasingly
challenged
disruptions
such
as
night
shifts,
late-night
activities,
jet
lag.
These
often
lead
rhythm
disorders,
which
now
being
linked
heart
diseases.
review
explored
potential
cardiovascular
system.
Beyond
its
regulation,
could
significantly
influence
physiological
pathological
related
health,
atherosclerosis,
ischemia/reperfusion
injury,
failure.
Mechanistically,
regulate
glucose
lipid
ferroptosis,
mitochondrial
function.
The
highlighted
protective
roles
underlying
mechanisms
diseases,
suggesting
multidisciplinary
research
may
provide
basis
breakthroughs
REV-ERB-targeted
therapies
disorders.
Cardiovascular Research,
Journal Year:
2025,
Volume and Issue:
unknown
Published: May 8, 2025
Abstract
Aims
The
prediction
of
atrial
fibrillation
(AF)
progression
and
post-ablation
recurrence
is
currently
based
on
empirical
estimates,
leading
to
suboptimal
predictive
accuracy.
This
study
investigates
whether
remodelling,
a
key
factor
in
the
severity
cardiomyopathy,
could
serve
as
shared
substrate
influencing
both
AF
recurrence.
We
aimed
identify
circular
RNAs
(circRNAs)
associated
with
remodelling
evaluate
their
ability
predict
Methods
results
assessed
differential
expression
plasma
circRNAs
between
paroxysmal
(PAF)
persistent
(PsAF)
patients
using
microarray
analysis.
Selected
candidate
were
validated
through
qPCR
following
rigorous
statistical
bioinformatics
circDGCR8
was
consistently
found
be
up-regulated
PsAF
compared
PAF
patients.
Additionally,
significantly
human
fibroblasts
treated
angiotensin
II
(AngII).
Gain-
loss-of-function
studies
suggested
that
promote
at
cellular
level
by
enhancing
collagen
production
fibroblast
proliferation.
Overexpression
cardiac
altered
gene
spectrum,
impacting
pathways
including
IL-17
signalling
TNF
signalling.
Moreover,
levels
positively
correlated
fibrosis,
indicated
increased
percentages
low
voltage
zones.
value
evaluated
two
cohorts:
(i)
monitored
for
36
months
endpoint,
(ii)
who
underwent
radiofrequency
ablation
followed
12
assess
In
cohorts,
higher
risks
Conclusion
Our
suggest
circDGCR8,
holds
potential
biomarker
PLoS ONE,
Journal Year:
2024,
Volume and Issue:
19(5), P. e0304041 - e0304041
Published: May 21, 2024
Ventricular
fibrillation
(VF)
in
acute
myocardial
infarction
(AMI)
is
the
main
cause
of
deaths
occurring
phase
an
ischemic
event.
Although
it
known
that
genetics
may
play
important
role
this
pathology,
possible
long
non-coding
RNAs
(lncRNA)
has
never
been
studied.
Therefore,
aim
work
to
study
expression
10
lncRNAs
patients
with
and
without
VF
AMI.
For
purpose,
CDKN2B-AS1,
KCNQ1OT1,
LIPCAR,
MALAT1,
MIAT,
NEAT1,
SLC16A1-AS1
,
lnc-TK2-4
:
2
TNFRSF14-AS1
UCA1
were
analyzed.
After
analysis
Bonferroni
correction,
lncRNA
CDKN2B-AS
showed
a
statistical
significance
lower
(P
values
2.514
x
−5
).
In
silico
revealed
six
proteins
could
be
related
effect
CDKN2B-AS1
AGO3,
PLD4,
POU4F1,
ZNF26,
ZNF326
ZNF431.
These
predicted
have
low
cardiac
expression,
although
there
no
literature
indicating
potential
relationship
Thus,
shows
significant
AMI
vs
Literature
data
suggest
CDKN2B1-AS
miR-181a/SIRT1
pathway.
The
embryonic
epicardium
originates
from
the
proepicardium,
an
extracardiac
primordium
constituted
by
a
cluster
of
mesothelial
cells.
In
early
embryos,
is
characterized
squamous
cell
epithelium
resting
on
myocardium
surface.
Subsequently,
it
invades
subepicardial
space
and
thereafter
means
epithelial-mesenchymal
transition.
Within
myocardium,
epicardial-derived
cells
present
multilineage
potential,
later
differentiating
into
smooth
muscle
contributing
both
to
coronary
vasculature
cardiac
fibroblasts
in
mature
heart.
Over
last
decades,
we
have
progressively
increased
our
understanding
those
cellular
molecular
mechanisms
driving
proepicardial/embryonic
formation.
This
study
provides
state-of-the-art
review
transcriptional
emerging
post-transcriptional
involved
formation
differentiation
epicardium.