Epigenetic regulation in coronary artery disease: from mechanisms to emerging therapies
Frontiers in Molecular Biosciences,
Journal Year:
2025,
Volume and Issue:
12
Published: Jan. 31, 2025
Atherosclerosis,
the
primary
cause
of
coronary
artery
disease
(CAD),
remains
a
leading
global
mortality.
It
is
characterized
by
accumulation
cholesterol-rich
plaques
and
inflammation,
which
narrow
arteries
increase
risk
rupture.
To
elucidate
this
complex
biological
process
improve
therapeutic
strategies,
CAD
has
been
extensively
explored
from
an
epigenetic
perspective
over
past
two
decades.
Epigenetics
field
investigating
heritable
alterations
in
gene
expression
without
DNA
sequence
changes,
such
as
methylation,
histone
modifications,
non-coding
RNAs.
Increasing
evidence
indicated
that
development
significantly
influenced
changes.
Meanwhile,
impact
epigenetics
now
transitioning
pathophysiology
to
therapeutics.
Focusing
on
key
enzymes
their
target
genes
will
help
facilitate
diagnosis
treatment
CAD.
This
review
synthesizes
novel
insights
into
CAD,
addressing
pathological
processes,
molecular
mechanisms,
potential
biomarkers.
Furthermore,
we
discuss
emerging
strategies
targeting
pathways.
By
focusing
pivotal
associated
genes,
work
aims
advance
diagnostics
interventions.
Language: Английский
Comparison and mechanism analysis of fatty acid differences between backcross F2 derived from blunt snout bream (Megalobrama amblycephala,♀) × topmouth culter (Culter alburnus,♂) and its closely related species
Qixiang Wang,
No information about this author
Haoyang Wangchen,
No information about this author
Jinhong Luo
No information about this author
et al.
Aquaculture International,
Journal Year:
2025,
Volume and Issue:
33(4)
Published: April 9, 2025
Language: Английский
Early and Late Responses of Cultured Human Mesenchymal Stem Cells (MSCs) to Cell-free DNA (cfDNA) in Patients With Acute Myocardial Infarction
Frontiers in Bioscience-Landmark,
Journal Year:
2025,
Volume and Issue:
30(4)
Published: March 31, 2025
Background:
Acute
myocardial
infarction
(AMI)
is
accompanied
by
damage
to
heart
tissues
and
some
cell
death.
Stem
cells
are
localized
in
the
affected
area
contribute
tissue
repair.
Studies
have
previously
shown
that
concentration
of
cell-free
DNA
(cfDNA)
blood
(ami-cfDNA)
increases
significantly
patients
with
AMI,
GC-rich
oxidized
fragments
accumulate
composition
ami-cfDNA.
As
a
result,
ami-cfDNA
exhibits
biological
activity
vitro
against
various
types
differentiated
human
cells.
Potentially,
can
influence
functional
direction
stem
differentiation.
To
verify
this
assumption,
we
investigated
effect
isolated
from
AMI
on
adipose
mesenchymal
(MSCs)
vitro.
Materials
Methods:
The
MSC
line
was
used
characterized
surface
markers.
Ami-cfDNA
control
(hc-cfDNA)
samples
were
plasma
seven
ten
healthy
donors.
early
(0.5–3
hours)
late
(1–3
weeks)
responses
MSCs
cfDNA
action
analyzed.
level
reactive
oxygen
species,
expression
numerous
genes
(NOX4,
NRF2,
BRCA1,
BCL2,
BAX,
MYOD1,
MYOG,
MYF5,
MRF4,
RUNX2,
SPP1,
OCN,
LPL,
AP2),
double-stranded
breaks
nuclei,
changes
spatial
organization
chromatin
nucleus
determined
using
quantitative
(real-time)
polymerase
chain
reaction
(qPCR),
flow
cytometry,
fluorescence
microscopy,
fluorescent
situ
hybridization
(FISH)
assays.
Results:
Introducing
into
culture
medium
stimulates
rapid
transient
induction
oxidative
stress
(early
response).
Oxidative
reorganization
develop
an
adaptive
response
(AR).
includes
antioxidant
anti-apoptotic
activation
repair
genes.
fragments,
unlike
hc-cfDNA,
stimulate
myogenic
differentiation
under
prolonged
exposure
(late
Conclusions:
survival
model
system
inducing
pronounced
cellular
response.
Prolonged
provokes
MSCs.
Under
acute
conditions
caused
body,
may
positively
affect
restoration
damaged
muscle.
Language: Английский