bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Дек. 11, 2024
ABSTRACT
Fibrosis
is
part
of
a
clinical
burden
in
cardiovascular
diseases.
The
pathological
process
has
been
the
subject
intensive
research
with
still
mitigated
therapeutic
options.
Recently
chromatin
modifiers
have
turned
out
to
be
potential
drugs
modulate
fibrosis.
Here,
order
address
question
pharmacological
inhibition
fibrosis,
we
used
both
mouse
model
myocardial
infarction
left
ventricular
fibrosis
and
more
clinically
relevant
pig
right
failure
featuring
interstitial
Treatment
these
diseased
animal
models
an
inhibitor
Lysine
Demethylase
1
(LSD1)
significantly
prevented
pig,
respectively.
This
was
revealed
by
significant
recovery
function
post-myocardial
limitation
remodeling
ventricle,
thus
preserving
its
function.
decreased
hearts,
which
likely
account
for
improvement
We
provide
evidence
beneficial
effect
LSD1
inhibitors
cardiac
use
such
preserve
ischemic
congenital
heart
NEW
&
NOTEWORTHY
Drugs
prevent
limited
outcomes.
work
inspired
oncology,
provides
that
epigenetic
modifier
targets
epithelial-to-mesenchymal
transition
turns
efficient
non-ischemic
Redox Biology,
Год журнала:
2024,
Номер
76, С. 103321 - 103321
Опубликована: Авг. 19, 2024
Cell
death
constitutes
a
critical
component
of
the
pathophysiology
cardiovascular
diseases.
A
growing
array
non-apoptotic
forms
regulated
cell
(RCD)-such
as
necroptosis,
ferroptosis,
pyroptosis,
and
cuproptosis-has
been
identified
is
intimately
linked
to
various
conditions.
These
RCD
are
governed
by
genetically
programmed
mechanisms
within
cell,
with
epigenetic
modifications
being
common
crucial
regulatory
method.
Such
include
DNA
methylation,
RNA
histone
acetylation,
non-coding
RNAs.
This
review
recaps
roles
modifications,
RNAs
in
diseases,
well
which
regulate
key
proteins
involved
death.
Furthermore,
we
systematically
catalog
existing
pharmacological
agents
targeting
novel
their
action
article
aims
underscore
pivotal
role
precisely
regulating
specific
pathways
thus
offering
potential
new
therapeutic
avenues
that
may
prove
more
effective
safer
than
traditional
treatments.
Frontiers in Cardiovascular Medicine,
Год журнала:
2025,
Номер
12
Опубликована: Апрель 8, 2025
With
the
global
impact
of
cardiovascular
disease,
there
is
a
dire
need
to
understand
mechanisms
in
heart
during
injury
and
stress.
It
has
been
shown
that
regulation
extracellular
matrix
via
cardiac
fibroblasts
plays
major
role
progression
failure
worsening
function
heart.
Importantly,
it
suggested
crosstalk
between
other
cells
like
cardiomyocytes,
immune
cells,
endothelial
are
influenced
by
pathological
fibroblasts.
This
decline
across
all
seemingly
irreversible.
However,
epigenetic
have
regulate
functionality
improve
outcomes
stress
or
injury.
also
control
communication
different
cell
types
influence
multiple
The
goal
this
review
summarize
discuss
current
research
subsequent
with
disease
states.
Theranostics,
Год журнала:
2025,
Номер
15(10), С. 4785 - 4807
Опубликована: Март 29, 2025
Background:
Atherosclerosis
is
a
chronic
inflammatory
disease
that
the
major
cause
of
mortality
worldwide.
Although
several
studies
have
assessed
function
m6A
(N6-methyladenosine)
modification
in
atherosclerosis,
its
regulatory
mechanism
at
single-cell
level
remains
unclear.
This
study
provides
comprehensive
atlas
regulating
cell-type-specific
functions
atherosclerosis.
Methods:
We
analyzed
sequencing
data
derived
from
atherosclerosis
patients
to
elucidate
influence
on
diverse
cell
types.
demonstrated
potential
regulators
across
various
types
and
key
transcription
factors
involved.
Furthermore,
we
discovered
mediated
intercellular
communication
important
biological
processes.
In
vitro
experiments
were
conducted
further
investigate
effects
ALKBH5,
WTAP
METTL3
Results:
ALKBH5
upregulated
endothelial
cells
induced
proliferation
migration
involved
sprouting
angiogenesis.
smooth
muscle
cells,
upregulation
enhanced
proliferation,
phenotypic
transformation.
Upregulation
YTHDF2
promoted
macrophage
activation
differentiation.
identified
abnormally
activated
could
regulate
manner.
Moreover,
revealed
implicated
dysregulated
And
series
experimental
validations
supported
conclusion
exert
functions.
Conclusion:
Our
provided
evidence
for
roles
orchestrating
atherosclerotic
functions,
representing
promising
targets
precision
medicine.
