Metformin decelerates aging clock in male monkeys
Cell,
Год журнала:
2024,
Номер
187(22), С. 6358 - 6378.e29
Опубликована: Сен. 12, 2024
Язык: Английский
Roles of chromatin and genome instability in cellular senescence and their relevance to ageing and related diseases
Nature Reviews Molecular Cell Biology,
Год журнала:
2024,
Номер
25(12), С. 979 - 1000
Опубликована: Окт. 3, 2024
Язык: Английский
Senolytic elimination of senescent cells improved periodontal ligament stem cell-based bone regeneration partially through inhibiting YAP
Biochimica et Biophysica Acta (BBA) - Molecular Cell Research,
Год журнала:
2025,
Номер
1872(3), С. 119921 - 119921
Опубликована: Фев. 18, 2025
Язык: Английский
Long Non-Coding RNA EPB41L4A-AS1 Serves as a Diagnostic Marker for Chronic Periodontitis and Regulates Periodontal Ligament Injury and Osteogenic Differentiation by Targeting miR-214-3p/YAP1
Journal of Inflammation Research,
Год журнала:
2025,
Номер
Volume 18, С. 2483 - 2497
Опубликована: Фев. 1, 2025
Several
long
non-coding
RNAs
(lncRNAs)
are
dysregulated
in
chronic
periodontitis
(CP).
The
study
aimed
to
elucidate
the
molecular
mechanisms
and
clinical
significance
of
lncRNA
EPB41L4A
antisense
RNA
1
(EPB41L4A-AS1)
CP.
This
enrolled
101
patients
with
CP
90
subjects
healthy
periodontal
tissues.
Patients
were
categorized
according
severity.
expression
EPB41L4A-AS1
osteogenic
markers
lipopolysaccharide
(LPS)-induced
human
ligament
cells
(hPDLCs)
was
assessed
using
real-time
quantitative
reverse
transcription
PCR
(RT-qPCR).
diagnostic
evaluated
receiver
operating
characteristic
(ROC)
analysis.
levels
inflammatory
factors
measured
an
enzyme-linked
immunosorbent
assay.
Cell
proliferation
apoptosis
analyzed
cell
counting
kit
-8
flow
cytometry,
respectively.
interaction
between
microRNAs
verified
dual
luciferase
reporter
assays,
immunoprecipitation,
pull-down
assays.
downregulated
gingival
sulcus
fluid
LPS-induced
hPDLCs.
Additionally,
could
distinguish
from
control
sensitivity
(88.12%)
specificity
(81.11%).
severe
downregulation
directly
correlated
indicators
inversely
indicators.
overexpression
promoted
differentiation
hPDLCs
mitigated
inflammation.
Mechanistically,
targets
downregulates
miR-214-3p
expression,
resulting
upregulation
Yes1-associated
transcriptional
regulator
(YAP1)
levels.
partially
suppressed
effects
on
hPDLC
injury
differentiation.
enhanced
through
miR-214-3p/YAP1
axis.
Thus,
is
a
novel
marker
therapeutic
target
for
Язык: Английский
Carnosine alleviates oxidative stress to prevent cellular senescence by regulating Nrf2/HO-1 pathway: a promising anti-aging strategy for oral mucosa
Frontiers in Pharmacology,
Год журнала:
2025,
Номер
16
Опубликована: Апрель 10, 2025
Introduction:
Aging
is
associated
with
significant
metabolic
alterations
that
contribute
to
cellular
senescence
and
age-related
functional
decline.
As
individuals
age,
an
increased
prevalence
of
oral
diseases
a
gradual
decline
in
functions
are
observed.
However,
the
shifts
underlying
mucosal
aging
remain
unexplored.
Methods:
We
initially
conducted
histological
analyses
on
tongues
from
young
(4-week-old),
adult
(4-month-old)
old
(20-month-old)
C57BL/6
mice
identify
tongue
mucosa.
Subsequently,
metabolomics
analysis
was
performed
characterize
profiles
mouse
across
these
age
groups
biomarkers
aging.
Then
we
validate
anti-senescence
effect
carnosine
investigate
its
mechanisms
using
tert-butyl
hydroperoxide
(tBHP)-induced
model
vitro.
Finally,
human
saliva
blood
were
explore
associations
between
levels
systemic
Results:
Compared
mice,
observed
epithelial
atrophy
accumulation
senescent
cells
mucosa
mice.
After
that,
found
differences
among
young,
adult,
tongues.
Carnosine
identified
as
potential
biomarker
aging,
declined
significantly
age.
Consistently,
synthase
1
(CARNS1)
activity
decreased,
carnosinase
2
(CNDP2)
Furthermore,
protected
tBHP-induced
by
reducing
oxidative
stress,
mitigating
DNA
damage,
downregulating
Nrf2/HO-1
pathway.
In
humans,
salivary
also
diseases.
Discussion:
Our
findings
reveal
dynamic
reprogramming
during
natural
highlight
dual
role
both
therapeutic
target
for
combating
degeneration.
These
insights
support
development
novel
carnosine-based
interventions
preserve
function,
prevent
diseases,
improve
health
population,
thereby
advancing
healthy
Язык: Английский
CRISPR screening uncovers nucleolar RPL22 as a heterochromatin destabilizer and senescence driver
Nucleic Acids Research,
Год журнала:
2024,
Номер
52(19), С. 11481 - 11499
Опубликована: Сен. 11, 2024
Dysfunction
of
the
ribosome
manifests
during
cellular
senescence
and
contributes
to
tissue
aging,
functional
decline,
development
aging-related
disorders
in
ways
that
have
remained
enigmatic.
Here,
we
conducted
a
comprehensive
CRISPR-based
loss-of-function
(LOF)
screen
ribosome-associated
genes
(RAGs)
human
mesenchymal
progenitor
cells
(hMPCs).
Through
this
approach,
identified
ribosomal
protein
L22
(RPL22)
as
foremost
RAG
whose
deficiency
mitigates
effects
senescence.
Consequently,
absence
RPL22
delays
hMPCs
from
becoming
senescent,
while
an
excess
accelerates
process.
Mechanistically,
found
senescent
hMPCs,
accumulates
within
nucleolus.
This
accumulation
triggers
cascade
events,
including
heterochromatin
decompaction
with
concomitant
degradation
key
proteins,
specifically
1γ
(HP1γ)
KRAB-associated
1
(KAP1).
Subsequently,
RPL22-dependent
breakdown
stimulates
transcription
RNAs
(rRNAs),
triggering
In
summary,
our
findings
unveil
novel
role
for
nucleolar
destabilizer
driver
senescence,
shedding
new
light
on
intricate
mechanisms
underlying
aging
Язык: Английский
Neuregulin-1 reduces Doxorubicin-induced cardiotoxicity by upregulating YAP to inhibit senescence
Henghe Shi,
Yifei Zou,
Yinghao Li
и другие.
International Immunopharmacology,
Год журнала:
2024,
Номер
143, С. 113278 - 113278
Опубликована: Окт. 14, 2024
The
cardiotoxicity
of
Doxorubicin
(Dox)
limits
its
clinical
application,
creating
an
urgent
need
to
investigate
underlying
mechanism
and
develop
effective
therapies.
Senescence
plays
important
role
in
Dox-induced
(DIC).
Recently,
Neuregulin-1
(NRG1)
was
found
regulate
Yes-associated
protein
(YAP),
which
reported
inhibit
senescence,
suggesting
that
NRG1
might
be
used
treat
DIC
by
inhibiting
senescence
through
YAP
regulation.
We
examined
the
changes
regulatory
roles
Dox
whether
could
reduce
chronic
mice
Dox-treated
H9c2
cells.
Our
study
revealed
sustained
small
doses
impaired
cardiac
function
cell
viability,
induced
myocardial
inhibited
expression.
Conversely,
high
levels
cells,
indicating
promotes
YAP.
In
addition,
we
exogenous
phosphorylation
LATS1
MST1,
thereby
promote
nuclear
translocation
YAP,
attenuating
cardiotoxicity.
knockdown
or
inhibition
binding
TEA
domain
transcription
factor
（TEAD）blocks
protective
effects
NRG1.
conclusion,
our
suggests
is
one
pathological
mechanisms
Additionally,
reduces
upregulating
senescence.
Язык: Английский