Clinical Science,
Journal Year:
2024,
Volume and Issue:
138(16), P. 991 - 1007
Published: Aug. 1, 2024
Abstract
Cellular
senescence
represents
a
condition
of
irreversible
cell
cycle
arrest,
characterized
by
heightened
senescence-associated
beta-galactosidase
(SA-β-Gal)
activity,
secretory
phenotype
(SASP),
and
activation
the
DNA
damage
response
(DDR).
Diabetic
kidney
disease
(DKD)
is
significant
contributor
to
end-stage
renal
(ESRD)
globally,
with
ongoing
unmet
needs
in
terms
current
treatments.
The
role
pathogenesis
DKD
has
attracted
substantial
attention
evidence
premature
this
condition.
process
cellular
appears
be
associated
mitochondrial
redox
pathways,
autophagy,
endoplasmic
reticulum
(ER)
stress.
Increasing
accumulation
senescent
cells
diabetic
not
only
leads
an
impaired
capacity
for
repair
injury,
but
also
secretion
pro-inflammatory
profibrotic
cytokines
growth
factors
causing
inflammation
fibrosis.
Current
treatments
diabetes
exhibit
varying
degrees
renoprotection,
potentially
via
mitigation
kidney.
Targeting
clearance
through
pharmaceutical
interventions
could
emerge
as
promising
strategy
preventing
treating
DKD.
In
paper,
we
review
understanding
summarize
possible
therapeutic
relevant
field.
Turkish Journal of Biochemistry,
Journal Year:
2025,
Volume and Issue:
unknown
Published: May 2, 2025
Abstract
Objectives
Calcium/Calmodulin-dependent
protein
kinase-2
(CaMKII)
is
a
serine/threonine
kinase
prevalent
in
neuronal
cells,
playing
key
role
memory,
learning,
and
synaptic
plasticity.
Nonspecific
CaMKII
inhibition
can
prevent
apoptosis
cells
reduce
glutamate-induced
cell
death.
Additionally,
variations
CaMKK
enzyme
levels
affect
hemopoietic
stem
proliferation,
although
the
effects
of
on
responses
during
stress
remain
unclear.
This
study
aims
to
explore
CaMKII’s
impact
survival
proliferation
mesenchymal
under
analyze
expression
its
isoforms
(alpha,
beta,
gamma,
delta)
these
conditions.
Methods
The
included
characterization
MSCs,
followed
by
an
evaluation
KN-93,
inhibitor,
viability
both
presence
absence
H
2
O
treatment.
toxicity
caused
application
1
mM
further
increased
inhibitor
Additionally
changes
gene
were
analyzed.
Results
significantly
decreased
total
CaMKII,
with
significant
reduction
delta
isoform.
Furthermore,
KN-93
induced
.
Viability
negatively
impacted
combined
treatment
compared
alone.
Conclusions
Our
findings
provide
strong
foundation
understand
response
mechanisms
MSCs
conditions
could
inform
strategies
for
targeted
therapies
oxidative
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(7), P. 817 - 817
Published: July 8, 2024
Periodontitis,
characterized
by
inflammation
and
loss
of
periodontal
tissue,
is
a
significant
health
complication
for
individuals
with
diabetes
mellitus
(DM).
Buildup
advanced
glycation
end-products
(AGEs)
in
DM
poses
an
increased
risk
periodontitis
via
inflammaging.
Ganoderma
immunomodulatory
protein
(GMI)
shows
promise
suppressing
inflammaging
mitigating
oxidative
stress
Nrf2
modulation.
However,
its
specific
protective
effects
are
not
fully
understood.
Thus,
this
study
aimed
to
investigate
GMI's
anti-inflammaging
properties
underlying
mechanism
diabetic-associated
(DP).
We
first
simulated
DP
culturing
human
gingival
fibroblasts
(HGFs)
AGEs
lipopolysaccharides
from
European Journal of Pharmacology,
Journal Year:
2024,
Volume and Issue:
980, P. 176865 - 176865
Published: July 30, 2024
Vitexin
is
a
natural
flavonoid
glycoside
compound
extracted
from
the
leaves
and
seeds
of
Vitex
negundo.
It
widely
distributed
in
stems
numerous
plants
exhibites
remarkable
anti-tumor,
anti-inflammatory,
anti-hypertensive
properties.
However,
whether
vitexin
presents
anti-aging
senescence
prevention
effect
has
not
been
fully
elucidated.
The
purpose
this
study
to
investigate
on
progeria
mice
cellular
senescence,
as
well
its
underlying
molecular
mechanisms.
To
generate
premature
aging/senescence
model
vivo
vitro,
we
used
D-galactose
(D-gal),
hydrogen
peroxide
(H
Clinical Science,
Journal Year:
2024,
Volume and Issue:
138(16), P. 991 - 1007
Published: Aug. 1, 2024
Abstract
Cellular
senescence
represents
a
condition
of
irreversible
cell
cycle
arrest,
characterized
by
heightened
senescence-associated
beta-galactosidase
(SA-β-Gal)
activity,
secretory
phenotype
(SASP),
and
activation
the
DNA
damage
response
(DDR).
Diabetic
kidney
disease
(DKD)
is
significant
contributor
to
end-stage
renal
(ESRD)
globally,
with
ongoing
unmet
needs
in
terms
current
treatments.
The
role
pathogenesis
DKD
has
attracted
substantial
attention
evidence
premature
this
condition.
process
cellular
appears
be
associated
mitochondrial
redox
pathways,
autophagy,
endoplasmic
reticulum
(ER)
stress.
Increasing
accumulation
senescent
cells
diabetic
not
only
leads
an
impaired
capacity
for
repair
injury,
but
also
secretion
pro-inflammatory
profibrotic
cytokines
growth
factors
causing
inflammation
fibrosis.
Current
treatments
diabetes
exhibit
varying
degrees
renoprotection,
potentially
via
mitigation
kidney.
Targeting
clearance
through
pharmaceutical
interventions
could
emerge
as
promising
strategy
preventing
treating
DKD.
In
paper,
we
review
understanding
summarize
possible
therapeutic
relevant
field.
