International Journal of Molecular Sciences,
Год журнала:
2023,
Номер
24(20), С. 15468 - 15468
Опубликована: Окт. 23, 2023
Aging
is
a
natural,
gradual,
and
inevitable
process
associated
with
series
of
changes
at
the
molecular,
cellular,
tissue
levels
that
can
lead
to
an
increased
risk
many
diseases,
including
cancer.
The
most
significant
genomic
level
(DNA
damage,
telomere
shortening,
epigenetic
changes)
non-genomic
are
referred
as
hallmarks
aging.
aging
cancer
intertwined.
Many
studies
have
focused
on
hallmarks,
but
also
important
may
additionally
cause
damage
increase
expression
hallmarks.
Understanding
cancer,
how
they
intertwined,
development
approaches
could
influence
these
thus
function
not
only
slow
prevent
In
this
review,
we
focus
changes.
We
discuss
cell
senescence,
disruption
proteostasis,
deregualation
nutrient
sensing,
dysregulation
immune
system
function,
intercellular
communication,
mitochondrial
dysfunction,
stem
exhaustion
dysbiosis.
Driven
by
genetic
and
environmental
factors,
aging
is
a
physiological
process
responsible
for
age-related
degenerative
changes
in
the
body,
cognitive
decline,
impaired
overall
wellbeing.
Notably,
premature
as
well
emergence
of
progeroid
syndromes
have
posed
concerns
regarding
chronic
health
conditions
comorbidities
population.
Accelerated
telomere
attrition
also
implicated
metabolic
dysfunction
development
disorders.
Impaired
homeostasis
arises
secondary
to
increases
synthesis
free
radicals,
decreased
oxidative
capacity,
antioxidant
defense,
disrupted
energy
metabolism.
In
particular,
several
cellular
molecular
mechanisms
been
identified
decipher
influence
on
diseases.
These
include
defective
DNA
repair,
attrition,
epigenetic
alterations,
dysregulation
nutrient-sensing
pathways.
The
role
pathogenesis
diseases
has
largely
attributed
pro-inflammatory
states
that
promote
shortening,
mutations
telomerase
reverse
transcriptase,
alteration,
stress,
mitochondrial
dysfunctions.
Nonetheless,
therapeutic
interventions
focus
restoring
length
telomeres
may
treatment
approaches
restore
enzyme
activity,
alternative
lengthening
telomeres,
counter
decrease
concentration
cytokines.
Given
significance
robust
potential
delaying
diseases,
this
review
aimed
explore
underlying
assimilating
evidence
from
both
human
animal
studies.
Abstract
Cellular
senescence
is
the
permanent
cessation
of
cell
proliferation
and
growth.
Senescent
cells
accumulating
in
tissues
organs
with
aging
contribute
to
many
chronic
diseases,
mainly
through
secretion
a
pro-inflammatory
senescence-associated
secretory
phenotype
(SASP).
Senotherapeutic
(senolytic
or
senomorphic)
strategies
targeting
senescent
or/and
their
SASP
are
being
developed
prolong
healthy
lifespan
treat
age-related
pathologies.
Sodium-glucose
co-transporter
2
(SGLT2)
inhibitors
new
class
anti-diabetic
drugs
that
promote
renal
excretion
glucose,
resulting
lower
blood
glucose
levels.
Beyond
glucose-lowering
effects,
SGLT2
have
demonstrated
protective
effects
against
cardiovascular
events.
Moreover,
recently
been
associated
inhibition
senescence,
making
them
promising
therapeutic
approach
for
aging.
This
review
examines
latest
research
on
senotherapeutic
potential
inhibitors.
Antioxidants,
Год журнала:
2025,
Номер
14(6), С. 691 - 691
Опубликована: Июнь 6, 2025
The
crosstalk
between
autophagy
and
oxidative
stress
is
a
cornerstone
of
stem
cell
biology.
These
processes
are
tightly
interwoven,
forming
regulatory
network
that
impacts
survival,
self-renewal,
differentiation.
Autophagy,
cellular
recycling
mechanism,
ensures
the
removal
damaged
organelles
proteins,
thereby
maintaining
integrity
metabolic
balance.
Oxidative
stress,
driven
by
accumulation
reactive
oxygen
species
(ROS),
can
act
as
both
signalling
molecule
source
damage,
depending
on
its
levels
context.
interplay
shapes
fate
either
promoting
survival
under
conditions
or
triggering
senescence
apoptosis
when
dysregulated.
Recent
evidence
underscores
bidirectional
relationship
these
processes,
where
mitigates
damage
degrading
ROS-generating
organelles,
induce
protective
response.
This
critical
not
only
for
preserving
function
but
also
addressing
age-related
decline
enhancing
regenerative
potential.
Understanding
molecular
mechanisms
govern
this
offers
novel
insights
into
biology
therapeutic
strategies.
review
delves
intricate
dynamics
in
cells,
emphasizing
their
synergistic
roles
health,
disease,
medicine
applications.
International Journal of Molecular Sciences,
Год журнала:
2023,
Номер
24(20), С. 15468 - 15468
Опубликована: Окт. 23, 2023
Aging
is
a
natural,
gradual,
and
inevitable
process
associated
with
series
of
changes
at
the
molecular,
cellular,
tissue
levels
that
can
lead
to
an
increased
risk
many
diseases,
including
cancer.
The
most
significant
genomic
level
(DNA
damage,
telomere
shortening,
epigenetic
changes)
non-genomic
are
referred
as
hallmarks
aging.
aging
cancer
intertwined.
Many
studies
have
focused
on
hallmarks,
but
also
important
may
additionally
cause
damage
increase
expression
hallmarks.
Understanding
cancer,
how
they
intertwined,
development
approaches
could
influence
these
thus
function
not
only
slow
prevent
In
this
review,
we
focus
changes.
We
discuss
cell
senescence,
disruption
proteostasis,
deregualation
nutrient
sensing,
dysregulation
immune
system
function,
intercellular
communication,
mitochondrial
dysfunction,
stem
exhaustion
dysbiosis.
