Drug and Chemical Toxicology,
Journal Year:
2025,
Volume and Issue:
unknown, P. 1 - 12
Published: May 28, 2025
This
study
investigates
the
molecular
mechanisms
underlying
anthracyclines
(ANT)-induced
cardiotoxicity,
with
a
specific
focus
on
ferroptosis
regulated
by
long
non-coding
RNA
(lncRNA)
H19/heme
oxygenase-1
(Hmox1)
signaling
axis.
A
retrospective
analysis
was
performed
50
breast
cancer
patients
who
developed
ANT-associated
cardiac
dysfunction.
Clinical
assessments
included
measurements
of
left
ventricular
ejection
fraction
(LVEF)
and
serum
markers,
such
as
troponin
I
(cTnI),
creatine
kinase-MB
(CK-MB),
N-terminal
pro-B-type
natriuretic
peptide
(NT-proBNP),
iron
levels.
Serum
revealed
marked
downregulation
lncRNA
H19
upregulation
Hmox1,
both
significantly
correlated
impaired
function
disrupted
homeostasis.
To
further
elucidate
mechanism,
an
Epirubicin
(EPI)-induced
injury
model
in
HL-1
cardiomyocytes
established.
EPI
exposure
led
to
suppression
H19,
induction
apoptosis
ferroptotic
cell
death.
RNA-seq
identified
potential
downstream
targets
linking
metabolism
via
Hmox1
modulation.
Functional
assays
demonstrated
that
overexpression
mitigated
EPI-induced
ferroptosis,
while
enforced
expression
reversed
these
protective
effects.
Collectively,
findings
identify
H19/Hmox1
axis
critical
regulator
ANT-induced
cardiotoxicity
suggest
it
therapeutic
target
for
mitigating
undergoing
anthracycline
chemotherapy.
Antioxidants and Redox Signaling,
Journal Year:
2024,
Volume and Issue:
40(7-9), P. 369 - 432
Published: Feb. 1, 2024
Physiological
levels
of
reactive
oxygen
and
nitrogen
species
(ROS/RNS)
function
as
fundamental
messengers
for
many
cellular
developmental
processes
in
the
cardiovascular
system.
ROS/RNS
involved
cardiac
redox-signaling
originate
from
diverse
sources,
their
are
tightly
controlled
by
key
endogenous
antioxidant
systems
that
counteract
accumulation.
However,
dysregulated
redox-stress
resulting
inefficient
removal
leads
to
inflammation,
mitochondrial
dysfunction,
cell
death,
contributing
development
progression
disease
(CVD).
MedComm,
Journal Year:
2025,
Volume and Issue:
6(3)
Published: March 1, 2025
Pulmonary
hypertension
(PH)
stands
as
a
tumor
paradigm
cardiovascular
disease
marked
by
hyperproliferation
of
cells
and
vascular
remodeling,
culminating
in
heart
failure.
Complex
genetic
epigenetic
mechanisms
collectively
contribute
to
the
disruption
pulmonary
homeostasis.
In
recent
years,
advancements
research
technology
have
identified
numerous
gene
deletions
mutations,
addition
bone
morphogenetic
protein
receptor
type
2,
that
are
closely
associated
with
remodeling
process
PH.
Additionally,
modifications
such
RNA
methylation,
DNA
histone
modification,
noncoding
RNAs
been
shown
precisely
regulate
PH
molecular
networks
cell-type-specific
manner,
emerging
potential
biomarkers
therapeutic
targets.
This
review
summarizes
analyzes
roles
currently
genes
factors
PH,
emphasizing
pivotal
role
long
ncRNAs
its
regulation.
it
examines
current
clinical
preclinical
therapies
for
targeting
these
explores
new
treatment
strategies.
Frontiers in Cardiovascular Medicine,
Journal Year:
2024,
Volume and Issue:
10
Published: Jan. 8, 2024
Heart
failure
with
preserved
ejection
fraction
(HFpEF)
is
the
largest
unmet
clinical
need
in
cardiovascular
medicine.
Despite
decades
of
research,
treatment
option
for
HFpEF
still
limited,
indicating
our
ongoing
incomplete
understanding
on
underlying
molecular
mechanisms.
Non-coding
RNAs,
comprising
microRNAs
(miRNAs),
long
non-coding
RNAs
(lncRNAs)
and
circular
(circRNAs),
are
non-protein
coding
RNA
transcripts,
which
implicated
various
diseases.
However,
their
role
pathogenesis
unknown.
Here,
we
discuss
miRNAs,
lncRNAs
circRNAs
that
involved
pathophysiology
HFpEF,
namely
microvascular
dysfunction,
inflammation,
diastolic
dysfunction
cardiac
fibrosis.
We
interrogated
evidence
dissected
mechanisms
ncRNAs
by
looking
at
relevant
vivo
vitro
models
mimic
co-morbidities
patients
HFpEF.
Finally,
potential
as
biomarkers
novel
therapeutic
targets
future
treatment.
Frontiers in Endocrinology,
Journal Year:
2025,
Volume and Issue:
16
Published: March 14, 2025
Diabetes
mellitus
is
a
major
risk
factor
for
myocardial
infarction
(MI),
yet
its
molecular
mechanisms
exacerbating
post-MI
cardiac
remodeling
remain
unclear.
Type
2
diabetes
mouse
model
was
developed
through
high-sugar
and
high-fat
diet
(HFD),
followed
by
MI
surgery.
Four
weeks
post-surgery,
function
evaluated
via
echocardiography,
pathology
examined
using
Masson's
trichrome
wheat
germ
agglutinin
staining.
High-throughput
sequencing
identified
differentially
expressed
mRNAs
long
non-coding
RNAs
(LncRNAs)
in
diabetic
mice
with
MI.
Gene
Ontology
(GO)
Kyoto
Encyclopedia
of
Genes
Genomes
(KEGG)
pathway
analyses,
along
LncRNA-target-gene
analysis,
were
performed.
Validation
human
samples
patients
STEMI
confirmed
the
influence
HFD
on
expression
specific
genes.
The
results
demonstrate
that
significantly
impairs
function,
exacerbates
fibrosis
hypertrophy.
In
addition,
our
extensive
examination
has
conclusively
demonstrated
modulates
genes
(Rapgef5
Ing1)
within
tissue
individuals
afflicted
STEMI,
underscoring
intricate
interplay
between
these
conditions.
we
have
found
Rapgef5
Ing1
are
involved
diabetes-mediated
cardiomyocyte
apoptosis
proliferation
following
infarction.
aggravates
Rapgef5/Ing1-mediated
proliferation,
findings
highlight
novel
therapeutic
targets
cardiovascular
complications.
Journal of Clinical Medicine,
Journal Year:
2025,
Volume and Issue:
14(8), P. 2846 - 2846
Published: April 21, 2025
Background/Objectives:
Air
pollution
is
the
highest
environmental
risk
factor
of
mortality
and
morbidity
worldwide,
leading
to
over
4
million
deaths
each
year.
Among
different
air
pollutants,
ultrafine
particles
(UFPs)
constitute
cardiovascular
diseases
(CVDs).
Epidemiological
studies
have
associated
UFPs
with
short-
long-term
imbalance
numerous
blood
markers.
Our
objective
was
systematically
review
short-term
impact
UFP
exposure
on
markers
CVDs.
Methods:
We
prepared
systematic
CVD
meta-analyses
effects
high-sensitivity
C-reactive
protein
(hsCRP)
concentration.
The
eligibility
criteria
were
established
use
Provider,
Enrollment,
Chain,
Ownership
System
(PECOS)
model,
literature
search
conducted
in
Web
Science,
PubMed,
Scopus
databases
from
1
January
2013
9
2025.
bias
(RoB)
according
a
World
Health
Organization
(WHO)
template.
Results:
results
showed
an
increase
hsCRP
as
result
both
UFPs.
Moreover,
IL-6
IL-1β
together
other
inflammatory
increased
after
exposure.
In
addition,
nucleic
acids,
among
which
miR-24-3p
let-7d-5p,
differentially
expressed
(DE)
Chronic
could
lead
persistent
Conclusions:
findings
underline
that
may
development
and/or
worsening
outcomes
fragile
populations
living
air-polluted
areas.
RNA Biology,
Journal Year:
2023,
Volume and Issue:
20(1), P. 334 - 347
Published: June 13, 2023
Psoriasis
is
a
chronic
inflammatory
skin
disease
characterized
by
infiltration
of
immune
cells
and
abnormal
epidermal
thickening.
The
initial
pathogenesis
has
not
been
fully
elucidated.
Non-coding
RNAs
(ncRNAs),
which
include
long
ncRNAs
(lncRNAs)
circular
(circRNAs),
comprise
the
majority
genome
transcripts
are
important
influencers
gene
transcription
post-transcription
modulations.
Emerging
roles
in
psoriasis
were
identified
recently.
This
review
summarizes
existing
studies
psoriasis-related
lncRNAs
circRNAs.
A
considerable
proportion
studied
circRNAs
regulate
keratinocyte
mobility,
such
as
proliferation
differentiation.
Some
tightly
related
to
inflammation
reactions.
Other
reports
demonstrated
that
they
also
implicated
modulating
cell
differentiation,
proliferation,
activation.
might
illuminate
future
research
highlight
act
therapeutic
targets.
Food & Function,
Journal Year:
2023,
Volume and Issue:
14(20), P. 9350 - 9363
Published: Jan. 1, 2023
Oxidative
stress
(OS)
is
an
important
trigger
of
vascular
endothelial
injury
(VEI),
which
then
leads
to
cardiovascular
disease
(CVDs).
Phloretin
was
previously
investigated
alleviate
OS
in
human
umbilical
vein
cells
(HUVECs)
by
activating
the
AMPK/Nrf2
pathway;
however,
whether
phloretin
exerts
health
benefits
targeting
non-coding
RNAs
(ncRNAs)
remains
unclear.
Herein,
whole
transcriptome
sequencing
and
lncRNA
library
building
were
performed
on
HUVECs,
a
commonly
used
cell
line
for
CVDs
study,
from
different
groups
control
(CK),
palmitic
acid
(PA,
100
μM),
PA
+
(50
μM,
G50).
KEGG
analysis
demonstrated
that
DE-lncRNAs
regulated
pathway
related
metabolism
HUVECs.
LncBAG6-AS
highly
expressed
under
stimulation,
reversed
co-treatment.
Moreover,
MMP,
activities
SOD,
GSH-Px,
T-AOC
GR
significantly
ameliorated
after
interference
LncBAG6-AS,
consistent
with
recover
group.
Furthermore,
expression
DE-genes
reported
mRNA
sequencing,
including
MAPK10,
PIK3R1,
ATP2B4,
AKT2,
ADCY9,
changed
interference,
indicating
may
participate
process
attenuation
through
regulating
gene
expression.
So,
HUVECs
knockdown
subsequently
"NC
vs.
si-ASO-LncBAG6-AS"
enriched
GO
terms,
such
as
apoptosis,
response
OS,
ferroptosis,
others,
similar
those
observed
analysis.
Overall,
this
study
provides
new
insights
into
molecular
mechanisms
bioactive
substances
potential
targets
early
prevention
treatment
VEI.