Physiological Research,
Journal Year:
2024,
Volume and Issue:
unknown
Published: March 22, 2024
RNA
modifications
affect
key
stages
of
the
life
cycle,
including
splicing,
export,
decay,
and
translation.
Epitranscriptomic
regulations
therefore
significantly
influence
cellular
physiology
pathophysiology.
Here,
we
selected
some
most
abundant
reviewed
their
roles
in
heart
cardiovascular
diseases:
N6-methyladenosine
(m6A),
N6,2'-O-dimethyladenosine
(m6Am),
N1-methyladenosine
(m1A),
pseudouridine
(?),
5
methylcytidine
(m5C),
inosine
(I).
Dysregulation
epitranscriptomic
machinery
affecting
these
vastly
changes
cardiac
phenotype
is
linked
with
many
diseases
such
as
myocardial
infarction,
cardiomyopathies,
or
failure.
Thus,
a
deeper
understanding
regulatory
mechanisms
can
enhance
our
knowledge
molecular
underpinnings
prevalent
diseases,
potentially
paving
way
for
novel
therapeutic
strategies.
Keywords:
Epitranscriptomics,
modifications,
Epigenetics,
m6A,
RNA,
Heart.
Biomedicine & Pharmacotherapy,
Journal Year:
2024,
Volume and Issue:
171, P. 116185 - 116185
Published: Jan. 18, 2024
Diabetic
kidney
disease
(DKD)
is
a
major
microvascular
complication
of
diabetes,
and
hyperglycemic
memory
associated
with
diabetes
carries
the
risk
occurrence,
even
after
termination
blood
glucose
injury.
The
existence
supports
concept
an
epigenetic
mechanism
involving
n6-methyladenosine
(m6A)
modification.
Several
studies
have
shown
that
m6A
plays
key
role
in
pathogenesis
DKD.
This
review
addresses
RNA
modification
progression
DKD,
including
regulatory
pathological
processes,
such
as
inflammation,
oxidative
stress,
fibrosis,
non-coding
(nc)
RNA.
reveals
importance
occurrence
development
suggesting
may
play
phenomenon.
also
discusses
how
some
gray
areas,
modified
multiple
enzymes,
interact
to
affect
DKD
provides
countermeasures.
In
conclusion,
this
enhances
our
understanding
from
perspective
modifications
new
targets
for
future
therapeutic
strategies.
addition,
insights
discussed
here
support
effects
which
far-reaching
implications
novel
treatments.
We
hypothesize
modification,
factor
regulating
in-depth
exploration
option
clinical
management
patients
Molecular Medicine,
Journal Year:
2025,
Volume and Issue:
31(1)
Published: Feb. 19, 2025
Abstract
Radiotherapy
is
one
of
the
most
effective
treatments
for
malignant
tumors.
Radioresistance
a
major
factor
that
contributes
to
radiotherapy
failure
and
poor
prognosis.
Recent
studies
have
elucidated
pivotal
role
aberrant
N6-methyladenosine
(m6A)
modification,
predominant
internal
mRNA
modification
in
eukaryotic
cells,
influences
cancer
progression
by
disrupting
gene
expression
other
critical
cellular
processes.
Furthermore,
m6A
methylation
provides
substrate
tumor
therapy;
however,
whether
it
regulates
radioresistance
remains
unclear.
Methylated
transferase
(writer),
demethylated
(eraser),
methylated
recognition
protein
(reader)
are
three
essential
proteins
regulate
via
different
mechanisms
This
review
summarizes
latest
research
advances
aims
provide
novel
perspectives
on
advancement
regimens
overcome
invasion.
Epigenetics,
Journal Year:
2023,
Volume and Issue:
18(1)
Published: June 18, 2023
Epitranscriptomic
modifications
have
recently
emerged
into
the
spotlight
of
researchers
due
to
their
vast
regulatory
effects
on
gene
expression
and
thereby
cellular
physiology
pathophysiology.
N6,2'-O-dimethyladenosine
(m6Am)
is
one
most
prevalent
chemical
marks
RNA
dynamically
regulated
by
writers
(PCIF1,
METTL4)
erasers
(FTO).
The
presence
or
absence
m6Am
in
affects
mRNA
stability,
regulates
transcription,
modulates
pre-mRNA
splicing.
Nevertheless,
its
functions
heart
are
poorly
known.
This
review
summarizes
current
knowledge
gaps
about
modification
regulators
cardiac
biology.
It
also
points
out
technical
challenges
lists
currently
available
techniques
measure
m6Am.
A
better
understanding
epitranscriptomic
needed
improve
our
molecular
regulations
which
may
lead
novel
cardioprotective
strategies.
Ecotoxicology and Environmental Safety,
Journal Year:
2023,
Volume and Issue:
262, P. 115174 - 115174
Published: June 22, 2023
Owing
to
their
potential
adverse
health
effects,
global
contamination
by
microplastics
(MPs)
has
attracted
increased
scientific
and
societal
concerns.
However,
in
vivo
studies
on
MP
toxicity,
along
with
its
effects
underlying
mechanisms,
remain
limited.
We
recently
found
that
non-coding
RNA
(ncRNAs)
contribute
MP-mediated
vascular
toxicity.
Moreover,
previous
have
identified
N6-methyladenosine
(m6A)
modifications
ncRNAs
as
influencing
factors
cardiovascular
disease.
whether
how
m6A
are
affected
MP-induced
cardiotoxicity
unknown.
Herein,
we
profiled
differentially
expressed
related
modification
profiles
MP-exposed
myocardial
tissue
using
sequencing
(RNA-seq)
methylated
immunoprecipitation
(MeRIP-seq).
First,
observed
MPs
accumulated
different
organs
upregulated
apoptosis
the
heart,
liver,
spleen,
kidney
cells.
Furthermore,
total
METTL3
levels
myocardium
after
exposure
MPs.
RNA-seq
results
revealed
392
lncRNAs
302
circRNAs
were
MP-treated
mouse
compared
control
group.
Gene
Ontology
Kyoto
Encyclopedia
of
Genes
Genomes
enrichment
analyses
showed
these
altered
closely
associated
endocytosis,
cellular
senescence,
cell
cycle
signaling
pathways,
which
may
cause
cardiotoxicity.
MeRIP-seq
data
distributions
abundances
circRNAs.
Additionally,
through
conjoint
analysis
two
high-throughput
datasets
both
expression
circ-Arfgef2
lncG3bp2
This
suggests
involved
Our
findings
a
better
understanding
new
molecular
targets
for
treating
cardiac
injury.
Frontiers in Immunology,
Journal Year:
2023,
Volume and Issue:
14
Published: Sept. 11, 2023
Pulmonary
arterial
hypertension
(PAH)
is
a
severe
progressive
disease
that
may
cause
early
right
ventricular
failure
and
eventual
cardiac
failure.
The
pathogenesis
of
PAH
involves
endothelial
dysfunction,
aberrant
proliferation
pulmonary
artery
smooth
muscle
cells
(PASMCs),
vascular
fibrosis.
Hypoxia
has
been
shown
to
induce
elevated
secretion
growth
factor
(VEGF),
leading
the
development
hypoxic
PAH.
However,
molecular
mechanisms
underlying
remain
incompletely
understood.
Programmed
cell
death
(PCD)
natural
regulated
by
certain
genes.
Emerging
evidence
suggests
apoptotic
resistance
contributes
Moreover,
several
novel
types
PCD,
such
as
autophagy,
pyroptosis,
ferroptosis,
have
reported
be
involved
in
Additionally,
multiple
diverse
epigenetic
including
RNA
methylation,
DNA
histone
modification,
non-coding
molecule-mediated
processes
strongly
linked
These
modifications
affect
expression
genes,
which
produce
important
changes
cellular
biological
processes,
PCD.
Consequently,
better
understanding
PCD
modification
will
provide
novel,
specific
therapeutic
strategies
for
diagnosis
treatment.
In
this
review,
we
aim
discuss
recent
advances
elucidate
role
regulating
hypoxia-induced
Redox Report,
Journal Year:
2025,
Volume and Issue:
30(1)
Published: Jan. 27, 2025
Myocardial
ischemia-reperfusion
injury
(MIRI)
is
a
highly
complex
disease
with
high
morbidity
and
mortality.
Studying
the
molecular
mechanism
of
MIRI
discovering
new
targets
are
crucial
for
future
treatment
MIRI.
We
constructed
rat
model
hypoxia/reoxygenation
(H/R)
cardiomyocytes
model.
RT-PCR
Western
blot
were
used
to
investigate
expression
fat
mass
obesity-associated
(FTO)
gene.
Electrocardiogram,
echocardiography,
triphenyltetrazolium
chloride
(TTC)
staining
hematoxylin-eosin
(HE)
assess
effect
FTO
overexpression.
The
generation
reactive
oxygen
species
(ROS)
levels
superoxide
dismutase
(SOD2),
mitochondrial
transcription
factor
(TFAM)
cytochrome
c
oxidase
I
(COXI)
detected
oxidative
stress
biogenesis.
RNA
immunoprecipitation
(RIP)
pulldown
assays
identify
interaction
PGC-1a.
m6A
dot
blot,
methylated
PCR
(MeRIP-PCR)
stability
analysis
analyze
regulation
methylation
PGC-1a
by
FTO.
was
downregulated
in
rats
H/R
induced
cardiomyocytes.
Overexpression
inhibited
ROS
level
increased
SOD2,
TFAM
COXI
vitro
vivo.
In
addition,
identified
as
downstream
target
enhanced
mRNA
through
removing
modification.
Our
study
revealed
role
regulates
biogenesis
via
MIRI,
which
may
provide
approach
mitigating
Epigenetics,
Journal Year:
2025,
Volume and Issue:
20(1)
Published: Feb. 7, 2025
Although
N6-methyladenosine
(m6A)
may
be
related
to
the
pathogenesis
of
fibrotic
process,
mechanism
m6A
modification
in
aging-related
idiopathic
pulmonary
fibrosis
(IPF)
remains
unclear.
Three-milliliter
venous
blood
was
collected
from
IPF
patients
and
healthy
controls.
MeRIP-seq
RNA-seq
were
utilized
investigate
differential
modification.
The
expressions
identified
regulator
target
gene
validated
using
MeRIP-qPCR
real-time
PCR.
Moreover,
we
established
an
animal
model
a
senescent
A549
cells
explore
associated
molecular
mechanism.
Our
study
provided
panorama
methylation
IPF.
Increased
peaks
(3756)
decreased
(4712)
observed
group.
association
analysis
showed
that
749
DEGs
affected
by
Among
regulators,
expression
METTL14
level
our
interested
DDIT4
significantly,
but
mRNA
higher
This
further
verified
bleomycin-induced
fibrosis.
At
cellular
level,
it
confirmed
might
participate
senescence
alveolar
epithelial
cells.
downregulation
inhibit
decay
reducing
mRNA,
leading
high
protein.
alterations
discovered
as
potential
intervention
for
epigenetic
These
results
pave
way
future
investigations
regarding
modifications
PubMed,
Journal Year:
2025,
Volume and Issue:
27(2), P. 242 - 247
Published: Feb. 15, 2025
Combined
allergic
rhinitis
and
asthma
syndrome
(CARAS)
is
one
of
the
common
chronic
airway
inflammatory
diseases
in
children.
With
development
epigenetics,
research
on
CARAS
has
gradually
extended
from
protein
levels
to
molecular
levels,
such
as
transcription
post-transcriptional
regulation.
N6-methyladenosine
(m6A)
methylation
ferroptosis
have
emerged
promising
hotspots
recent
years,
playing
crucial
roles
tumors,
growth
development,
diseases.
This
paper
aims
summarize
characteristics
m6A
ferroptosis,
along
with
their
onset
progression
children,
thereby
providing
new
insights
strategies
for
diagnosis
treatment
childhood
CARAS.