Cancer
continues
to
place
a
heavy
burden
on
healthcare
systems
around
the
world.
Although
cancer
survivorship
improve,
cardiotoxicity
leading
cardiomyopathy
and
heart
failure
as
consequence
of
therapy
is
rising,
yesterday's
survivors
are
fast
becoming
today's
patients.
mechanisms
driving
complex,
cellular
senescence
gaining
attention
major
contributor
chemotherapy-induced
and,
therefore,
may
also
represent
novel
therapeutic
target
prevent
this
disease.
Cellular
well-recognized
response
clinical
doses
chemotherapies,
including
anthracyclines,
defined
by
cell
cycle
exit,
phenotypic
alterations
which
include
mitochondrial
dysfunction,
expression
pro-senescent,
pro-fibrotic,
pro-inflammatory
senescence-associated
phenotype.
Senescence
has
an
established
involvement
in
promoting
myocardial
remodeling
during
aging,
studies
have
demonstrated
that
elimination
can
attenuate
pathophysiology
several
cardiovascular
diseases.
Most
recently,
pharmacology-mediated
senescence,
using
class
drugs
termed
senolytics,
been
dysfunction
preclinical
models
cardiotoxicity.
In
review,
we
will
discuss
evidence
anthracycline-induced
causes
long-term
anticancer
consider
how
senescent
phenotype
promote
examine
exciting
possibility
targeting
prove
strategy
or
even
reverse
cardiac
dysfunction.
Cells,
Год журнала:
2025,
Номер
14(7), С. 499 - 499
Опубликована: Март 27, 2025
Cellular
senescence
is
an
irreversible
state
of
cell
cycle
arrest.
Senescent
cells
(SCs)
accumulate
in
the
body
with
age
and
secrete
harmful
substances
known
as
senescence-associated
secretory
phenotype
(SASP),
causing
chronic
inflammation;
at
same
time,
inflammation
leads
to
a
decrease
immune
system
function,
immunosenescence,
which
further
accelerates
aging
process.
immunosenescence
are
closely
related
variety
diseases,
including
cardiovascular
metabolic
disorders,
autoimmune
neurodegenerative
diseases.
Studying
mechanisms
cellular
developing
targeted
interventions
crucial
for
improving
function
quality
life
elderly
people.
Here,
we
review
series
recent
studies
focusing
on
molecular
regulation
by
system,
latest
advances
basic
clinical
research
senolytics.
We
summarize
animal
models
research,
well
mechanisms,
strategies,
future
directions
from
immunological
perspective,
hope
laying
foundation
novel
practical
anti-aging
therapies.
Aging and Disease,
Год журнала:
2023,
Номер
unknown
Опубликована: Янв. 1, 2023
The
aging
of
the
global
population
poses
significant
scientific
challenges.
Moreover,
biological
process
is
most
risk
factor
for
chronic
illnesses;
therefore,
understanding
molecular
and
cellular
mechanisms
underlying
these
aging-related
challenges
crucial
extending
healthy
lifespan
older
individuals.
Preventing
brain
remains
a
priority
public
health
goal,
integrative
comprehensive
analyses
have
revealed
that
immunosenescence
potential
cause
age-related
damage
disease
(e.g.,
stroke).
Importantly,
neuroinflammatory
immune
systems
present
two-way
contact
thus
can
affect
each
other.
Emerging
evidence
supports
numerous
effects
immunosenescence-
inflammation-mediated
immunity
in
neurologically
injured
brains.
In
this
study,
we
briefly
outline
how
alters
pathophysiology
transcriptional
amplitude
patients
who
experienced
stroke
then
discuss
system
its
components
are
affected
by
age
after
stroke.
Finally,
highlight
emerging
interventions
with
to
slow
down
or
reduce
prevent
onset.
Journal of Extracellular Vesicles,
Год журнала:
2023,
Номер
13(1)
Опубликована: Дек. 27, 2023
Abstract
Retinal
degeneration
(RD),
a
group
of
diseases
leading
to
irreversible
vision
loss,
is
characterised
by
retinal
pigment
epithelium
(RPE)
or
neuron
damage
and
loss.
With
fewer
risks
immune
rejection
tumorigenesis,
stem
cell‐secreted
extracellular
vesicles
(EVs)
offer
new
cell‐free
therapeutic
paradigm
for
RD,
which
remains
be
investigated.
Human
organoid‐derived
progenitor
cells
(hERO‐RPCs)
are
an
easily
accessible
advanced
cell
source
RD
treatment.
However,
hERO‐RPCs‐derived
EVs
require
further
characterisation.
Here,
we
compared
the
characteristics
from
hERO‐RPCs
(hRPC‐EVs)
with
those
human
embryonic
(hESC)‐derived
(hESC‐EVs)
as
controls.
Based
on
in‐depth
proteomic
analysis,
revealed
remarkable
differences
between
hRPC‐EVs
hESC‐EVs.
A
comparison
their
respective
origin
demonstrated
that
protein
loading
was
more
selective
than
In
particular,
hESC‐EVs
were
enriched
proteins
related
angiogenesis
cycle,
whereas
associated
modulation
development.
More
importantly,
hESC‐EVs,
exhibited
lower
correlation
proliferation
unique
capacity
regulate
lipid
metabolism.
It
confirmed
potentially
eliminated
deposits,
inhibited
lipotoxicity
oxidative
stress,
enhanced
phagocytosis
survival
oleic
acid‐treated
ARPE‐19
cells.
Mechanistically,
integrated
into
mitochondrial
network
cells,
increased
level
fatty
acid
β‐oxidation‐related
proteins.
Thus,
represent
promising
therapy
especially
blinding
abnormal
metabolism
in
RPE
Orthopaedic Surgery,
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 23, 2025
ABSTRACT
Objective
Knee
osteoarthritis
(KOA)
is
characterized
by
structural
changes.
Aging
a
major
risk
factor
for
KOA.
Therefore,
the
objective
of
this
study
was
to
examine
role
genes
related
aging
and
circadian
rhythms
in
Methods
This
identified
differentially
expressed
(DEGs)
comparing
gene
expression
levels
between
normal
KOA
samples
from
GEO
database.
Subsequently,
we
intersected
DEGs
with
aging‐related
rhythm
obtain
set
aging‐associated
Next,
conducted
Mendelian
randomization
(MR)
analysis,
using
as
exposure
factors,
their
SNPs
instrumental
variables,
outcome
event,
explore
causal
relationship
these
We
then
performed
Gene
Set
Enrichment
Analysis
(GSEA)
investigate
pathways
associated
selected
biomarkers,
immune
infiltration
built
competing
endogenous
RNA
(ceRNA)
network,
molecular
docking
studies.
Additionally,
findings
functional
roles
biomarkers
were
further
validated
through
experiments
on
human
cartilage
tissue
cell
models.
Results
A
total
75
aging‐circadian
group
difference
primarily
enriched
pathway.
Two
(PFKFB4
DDIT4)
screened
MR
analysis.
Then,
analysis
showed
significant
differences
three
types
cells
(resting
dendritic
cells,
resting
mast
M2
macrophages),
groups.
Drug
prediction
results
indicated
stable
binding
PFKFB4
estradiol
bisphenol_A,
while
DDIT4
binds
stably
nortriptyline
trimipramine.
Finally,
lines
established
lentiviral
infection
resistance
screening,
significantly
elevated
overexpressing
reversed
proliferation
migration
ability
after
IL‐1
β
treatment.
Conclusions
diagnostic
therapeutic
identified.
Functional
mechanism
exploration,
experimental
validation
elucidated
KOA,
offering
novel
perspectives
prevention
treatment
disease.
Cellular
senescence
has
been
identified
as
a
potential
driver
of
age-associated
loss
organ
function
and
mediator
age-related
disease.
Novel
strategies
in
targeting
senescent
cells
have
shown
promise
several
systems
to
counteract
functional
decline,
chronic
inflammation,
age-dependent
repair
capacity.
Transgenic
models
provided
proof
principle
that
senolysis,
the
elimination
cells,
is
an
attractive
strategy
overcome
many
pathologies.
The
translation
into
clinical
application
now
possible
with
emergence
drug-based
senotherapies.
In
this
review,
we
will
discuss
different
senotherapeutic
approaches
their
modes
action.
Senolytics
eliminate
preferentially
through
induction
apoptosis
but
not
normal
whereas
senomorphics
rather
interact
proinflammatory
profile
present
cells.
context
transplantation,
natural
clearance
might
be
reduced
because
dysfunctional
immune
surveillance
under
immunosuppression.
transplantation
setting
allows
for
applications
Conditioning
donor
organs
before
during
ex
situ
phase
offers
opportunity
interfere
accumulating
senescence,
ultimately
reducing
burden
life-limiting
comorbidities
chronically
ill
recipients.
Genes,
Год журнала:
2025,
Номер
16(4), С. 365 - 365
Опубликована: Март 22, 2025
Background:
Metformin
is
a
widely
used
oral
hypoglycemic
agent
for
treating
type
2
diabetes.
Planarians,
with
their
remarkable
regenerative
abilities,
are
frequently
employed
as
model
organisms
in
stem
cell
and
regeneration
studies.
This
study
aimed
to
investigate
the
effects
of
metformin
on
planarian
regeneration,
focusing
eyespots
after
amputation.
Methods:
Regenerating
planarians
amputated
were
exposed
various
concentrations
metformin.
The
time
was
measured
assess
Subsequently,
1
mmol/L
treatment
24
h
applied
planarians,
followed
by
transcriptome
analysis
identify
differentially
expressed
genes
(DEGs).
gene
expression
validated
through
qPCR.
full-length
casein
kinase
1α
(DjCK1α)
cloned
using
RACE
technology.
DjCK1α
interference
performed
examine
its
role
regeneration.
Results:
Low
significantly
reduced
planarians.
Transcriptome
identified
113
DEGs,
including
61
upregulated
52
downregulated
genes.
GO
KEGG
enrichment
analyses
conducted.
Notably,
DjCK1α,
key
involved
selected
further
validation.
qPCR
confirmed
that
upregulated.
prolonged
cultured
water,
while
did
not
promote
eyespot
DjCK1α-interfered
Conclusions:
results
suggest
accelerates
potentially
regulation
DjCK1α.
provides
first
transcriptome-based
drug
highlighting
process.
