Biogerontology,
Journal Year:
2024,
Volume and Issue:
25(5), P. 749 - 773
Published: July 1, 2024
Abstract
The
accumulation
of
pro-inflammatory
senescent
cells
within
tissues
is
a
common
hallmark
the
aging
process
and
many
age-related
diseases.
This
modification
has
been
called
senescence-associated
secretory
phenotype
(SASP)
observed
in
cultured
isolated
from
aged
tissues.
Currently,
there
debate
whether
should
be
attributed
to
increased
generation
or
defect
their
elimination
Emerging
studies
have
revealed
that
display
an
expression
several
inhibitory
immune
checkpoint
ligands,
especially
those
programmed
cell
death
protein-1
(PD-1)
ligand-1
(PD-L1)
proteins.
It
known
PD-L1
cancer
cells,
target
PD-1
receptor
cytotoxic
CD8
+
T
natural
killer
(NK)
disturbing
functions,
e.g.,
evoking
decline
activity
promoting
exhaustion
even
apoptosis.
An
increase
level
protein
was
able
suppress
surveillance
inhibit
by
NK
cells.
Senescent
are
express
ligands
for
receptors,
i.e.,
PD-1,
LILRB4,
NKG2A,
TIM-3,
SIRPα
receptors.
Here,
I
will
briefly
describe
pathways
examine
these
checkpoints
could
involved
evasion
with
seems
plausible
enhanced
signaling
can
prevent
thus
promote
process.
Journal of Oral Biology and Craniofacial Research,
Journal Year:
2024,
Volume and Issue:
14(3), P. 231 - 237
Published: March 13, 2024
Salivary
gland
hypofunction
is
highly
prevalent
in
aged
and
diseased
individuals
leading
to
significant
discomfort
morbidity.
One
factor
that
contributes
salivary
cellular
aging,
or
senescence.
Senescent
cells
can
impair
function
by
secreting
paracrine-acting
growth
factors
cytokines,
known
as
senescence-associated
secretory
phenotype
(SASP)
factors.
These
SASP
stimulate
inflammation,
propagate
the
senescent
through
bystander
effect,
fibrosis.
As
senotherapeutics
target
have
shown
effectiveness
limiting
disease
manifestations
other
conditions,
there
interest
use
of
these
drugs
treat
hypofunction.
In
this
review,
we
highlight
contribution
senescence
fibrosis
pathologies.
We
also
discuss
therapeutic
approaches
eliminate
modulate
for
treating
age-related
diseases
extending
health
span.
Biomedicines,
Journal Year:
2024,
Volume and Issue:
12(6), P. 1331 - 1331
Published: June 14, 2024
In
systemic
sclerosis
(SSc,
or
scleroderma),
defective
angiogenesis,
clinically
manifesting
with
abnormal
capillary
architecture
and
severe
reduction,
represents
a
hallmark
of
early-stage
disease,
usually
preceding
the
onset
tissue
fibrosis,
is
caused
by
several
cellular
molecular
mechanisms
affecting
microvascular
endothelial
cells
different
outcomes.
Indeed,
once
damaged,
can
be
dysfunctionally
activated,
thus
becoming
unable
to
undergo
angiogenesis
promoting
perivascular
inflammation.
They
also
apoptosis,
transdifferentiate
into
profibrotic
myofibroblasts,
acquire
senescence-associated
secretory
phenotype
characterized
release
exosomes
proinflammatory
mediators.
this
narrative
review,
we
aimed
give
comprehensive
overview
recent
studies
dealing
underlying
SSc
related
cell
dysfunctions,
mainly
endothelial-to-mesenchymal
transition
process.
We
discussed
potential
novel
vascular
treatment
strategies
able
restore
angiogenic
process
reduce
in
complex
disease.
Antioxidants,
Journal Year:
2025,
Volume and Issue:
14(2), P. 199 - 199
Published: Feb. 10, 2025
Aging
is
a
general
biological
process
inherent
in
all
living
organisms.
It
characterized
by
progressive
cellular
dysfunction.
For
many
years,
aging
has
been
widely
recognized
as
highly
effective
mechanism
for
suppressing
the
progression
of
malignant
neoplasms.
However,
recent
increasing
evidence
suggests
“double-edged”
role
cancer
development.
According
to
these
data,
not
only
tumor
suppressor
that
leads
cell
cycle
arrest
neoplastic
cells,
but
also
promoter
ensures
chronic
proinflammatory
and
immunosuppressive
microenvironment.
In
this
regard,
our
review,
we
discuss
data
on
destructive
senescent
cells
pathogenesis
cancer.
We
identify
first
time
correlations
between
modulation
senescence-associated
secretory
phenotype
antitumor
effects
naturally
occurring
molecules.
Journal of Hypertension,
Journal Year:
2025,
Volume and Issue:
unknown
Published: March 10, 2025
Background
and
purpose:
Ponatinib,
a
tyrosine
kinase
inhibitor
(TKI)
leads
to
hypertension;
however,
the
mechanisms
remain
elusive.
We
aimed
investigate
whether
lysine
acetyltransferase
7
(KAT7),
key
regulator
of
cellular
senescence
that
is
closely
associated
with
cardiovascular
diseases,
involves
in
ponatinib-induced
hypertension.
Methods
results:
After
administering
ponatinib
Sprague–Dawley
(SD)
rats
for
8
days,
we
measured
blood
pressure,
vasodilation,
endothelial
function
using
tail-cuff
plethysmography,
isometric
myography,
Total
NO
Assay
kit,
respectively.
The
results
indicated
increased
impaired
endothelium-dependent
relaxation
(EDR),
caused
injury
cells
SD
rats.
Furthermore,
PCR
Western
blot
experiments
demonstrated
an
upregulation
KAT7
expression
rat
mesenteric
artery
(MAECs)
following
treatment.
To
further
study
role
hypertension,
divided
into
four
groups:
control,
ponatinib,
WM-3835
(a
inhibitor),
plus
WM-3835.
Notably,
administration
significantly
improved
hypertension
EDR
dysfunction
Mechanistically,
over-expression
(OE-KAT7)
MAECs
led
inflammation,
phenomena
were
also
observed
arteries
ponatinib-treated
exposed
ponatinib.
However,
mitigated
these
detrimental
effects
both
vivo
vitro
experiments.
Additionally,
OE-KAT7
treatment
induced
H3K14
acetylation
(H3K14ac),
elevating
recruitment
H3K14ac
p21
promoter.
Moreover,
BAY
11-7085,
nuclear
factor
(NF)-κB
inhibitor,
potently
alleviated
accumulation
IL-6
IL-8,
as
well
cell
by
overexpression.
Conclusion:
Our
data
indicate
elevation
inflammatory
responses
through
NF-κB
signaling
pathway,
subsequently
vasotoxicity
