Epigenetic Mechanisms in the Transfer of Metabolic Disorders: A Comprehensive Review
Cureus,
Год журнала:
2025,
Номер
unknown
Опубликована: Март 11, 2025
Epigenetic
modifications,
including
deoxyribonucleic
acid
(DNA)
methylation,
histone
and
non-coding
ribonucleic
(ncRNAs),
regulate
gene
expression
without
altering
the
DNA
sequence
play
pivotal
roles
in
pathogenesis
of
metabolic
disorders
(MDs),
such
as
diabetes,
obesity,
cardiovascular
diseases.
This
review
aims
to
consolidate
current
knowledge
on
epigenetic
mechanisms
underlying
MDs,
emphasizing
modifications
ncRNAs.
A
comprehensive
literature
search
was
conducted
using
PubMed,
Scopus,
Web
Science
databases.
Studies
published
between
2000
2024
(a
few
foundational
historical
articles
were
also
added)
screened
terms
"epigenetics
AND
disorders,"
"DNA
methylation
diabetes,"
"histone
obesity,"
"non-coding
RNA
diseases."
Relevant
translational
clinical
studies
reviewed
synthesize
existing
evidence
regulation
Histone
acetylation,
phosphorylation,
ubiquitination,
contribute
dysregulation
by
modulating
chromatin
accessibility
transcription.
Additionally,
ncRNAs,
microRNAs,
long
circular
RNAs,
influence
pathways
post-transcriptionally
regulating
key
genes
involved
insulin
resistance,
lipid
metabolism,
inflammation.
Emerging
research
highlights
potential
biomarkers
for
early
disease
detection
prognosis,
well
therapeutic
modulators,
deacetylase
inhibitors
methylation-targeting
agents.
Despite
promising
advances,
challenges
remain
translating
findings
into
practice
because
inter-individual
variability
complex
interplay
genetics
environmental
factors.
Future
should
focus
large-scale,
multicenter
validate
develop
personalized
interventions
MDs.
Язык: Английский
The Inhibition of Bromodomain and Extraterminal Domain (BET) Proteins Protects Against Microglia-Mediated Neuronal Loss In Vitro
Biomolecules,
Год журнала:
2025,
Номер
15(4), С. 528 - 528
Опубликована: Апрель 4, 2025
Neuroinflammation
is
a
key
feature
of
all
neurodegenerative
disorders,
including
Alzheimer’s
disease,
and
tightly
regulated
by
epigenetic
mechanisms.
Among
them,
bromodomain
extraterminal
domain
(BET)
proteins
play
crucial
role
recognizing
acetylated
histones
acting
as
transcriptional
co-regulators
to
modulate
gene
expression.
This
study
investigates
the
potential
inhibiting
BET
in
preventing
microglia-mediated
neuronal
damage
vitro.
Murine
BV2
microglial
cells
were
exposed
lipopolysaccharide
(LPS)
or
amyloid-β
(Aβ)
induce
an
inflammatory
response,
subsequent
effects
on
murine
HT22
examined.
tested,
only
Brd4
was
significantly
upregulated
upon
pro-inflammatory
stimulation.
JQ1,
potent
pan-inhibitor
proteins,
suppressed
LPS-induced
upregulation
cytokine
mRNA
levels,
Il1b,
Il6,
Tnf,
microglia.
Pre-treatment
with
JQ1
attenuated
cytotoxicity
LPS-activated
toward
neurons.
Additionally,
conditioned
media
from
Aβ
fibril-stimulated
induced
cell
death,
which
partially
prevented
pre-treatment
JQ1.
Co-culture
assays
further
demonstrated
beneficial
effect
inhibition.
Our
findings
suggest
that
targeting
may
offer
neuroprotective
strategy
modulating
activation,
potentially
providing
therapeutic
benefits
diseases.
Язык: Английский