Frontiers in Molecular Biosciences,
Journal Year:
2025,
Volume and Issue:
11
Published: Jan. 28, 2025
Aging
and
cancer
are
intricately
linked
through
shared
molecular
processes
that
influence
both
the
onset
of
malignancy
progression
age-related
decline.
As
organisms
age,
cellular
stress,
genomic
instability,
an
accumulation
senescent
cells
create
a
pro-inflammatory
environment
conducive
to
development.
Autophagy,
process
responsible
for
degrading
recycling
damaged
components,
plays
pivotal
role
in
this
relationship.
While
autophagy
acts
as
tumor-suppressive
mechanism
by
preventing
organelles
proteins,
often
exploit
it
survive
under
conditions
metabolic
stress
treatment
resistance.
The
interplay
between
aging,
cancer,
reveals
key
insights
into
tumorigenesis,
senescence,
proteostasis
dysfunction.
This
review
explores
connections
these
processes,
emphasizing
potential
autophagy-targeted
therapies
strategies
could
be
further
explored
aging
treatment.
Understanding
dual
roles
suppressing
promoting
offers
promising
avenues
therapeutic
interventions
aimed
at
improving
outcomes
elderly
patients
while
addressing
deterioration.
Journal of Neuroinflammation,
Journal Year:
2024,
Volume and Issue:
21(1)
Published: April 2, 2024
Abstract
Background
Senescent
astrocytes
play
crucial
roles
in
age-associated
neurodegenerative
diseases,
including
Parkinson’s
disease
(PD).
Metformin,
a
drug
widely
used
for
treating
diabetes,
exerts
longevity
effects
and
neuroprotective
activities.
However,
its
effect
on
astrocyte
senescence
PD
remains
to
be
defined.
Methods
Long
culture-induced
replicative
model
1-methyl-4-phenylpyridinium/α-synuclein
aggregate-induced
premature
model,
mouse
of
were
investigate
the
metformin
vivo
vitro.
Immunofluorescence
staining
flow
cytometric
analyses
performed
evaluate
mitochondrial
function.
We
stereotactically
injected
AAV
carrying
GFAP-promoter-cGAS-shRNA
substantia
nigra
pars
compacta
regions
specifically
reduce
astrocytic
cGAS
expression
clarify
potential
molecular
mechanism
by
which
inhibited
PD.
Results
showed
that
vitro
mice.
Mechanistically,
normalized
function
DNA
release
through
mitofusin
2
(Mfn2),
leading
inactivation
cGAS-STING,
delayed
prevented
neurodegeneration.
Mfn2
overexpression
reversed
inhibitory
role
cGAS-STING
activation
senescence.
More
importantly,
ameliorated
dopamine
neuron
injury
behavioral
deficits
mice
reducing
accumulation
senescent
via
inhibition
activation.
Deletion
abolished
suppressive
Conclusions
This
work
reveals
delays
inhibiting
Mfn2-cGAS
suggest
is
promising
therapeutic
agent
diseases.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(10), P. 5122 - 5122
Published: May 8, 2024
While
primarily
produced
in
the
pineal
gland,
melatonin's
influence
goes
beyond
its
well-known
role
regulating
sleep,
nighttime
metabolism,
and
circadian
rhythms,
field
of
chronobiology.
A
plethora
new
data
demonstrates
melatonin
to
be
a
very
powerful
molecule,
being
potent
ROS/RNS
scavenger
with
anti-inflammatory,
immunoregulatory,
oncostatic
properties.
Melatonin
metabolites
exert
multiple
beneficial
effects
cutaneous
systemic
aging.
This
review
is
focused
on
neuroprotective
during
has
an
anti-aging
capacity,
retarding
rate
healthy
brain
aging
development
age-related
neurodegenerative
diseases,
such
as
Alzheimer's
disease,
Parkinson's
Huntington's
sclerosis,
amyotrophic
lateral
etc.
Melatonin,
well
metabolites,
N1-acetyl-N2-formyl-5-methoxykynuramine
(AFMK)
N1-acetyl-5-methoxykynuramine
(AMK),
can
reduce
oxidative
damage
by
shielding
mitochondria
from
dysfunction
process.
could
also
implicated
treatment
conditions,
modifying
their
characteristic
low-grade
neuroinflammation.
It
either
prevent
initiation
inflammatory
responses
or
attenuate
ongoing
inflammation.
Drawing
current
knowledge,
this
discusses
potential
benefits
supplementation
preventing
managing
cognitive
impairment
diseases.
Signal Transduction and Targeted Therapy,
Journal Year:
2025,
Volume and Issue:
10(1)
Published: March 7, 2025
Redox
signaling
acts
as
a
critical
mediator
in
the
dynamic
interactions
between
organisms
and
their
external
environment,
profoundly
influencing
both
onset
progression
of
various
diseases.
Under
physiological
conditions,
oxidative
free
radicals
generated
by
mitochondrial
respiratory
chain,
endoplasmic
reticulum,
NADPH
oxidases
can
be
effectively
neutralized
NRF2-mediated
antioxidant
responses.
These
responses
elevate
synthesis
superoxide
dismutase
(SOD),
catalase,
well
key
molecules
like
nicotinamide
adenine
dinucleotide
phosphate
(NADPH)
glutathione
(GSH),
thereby
maintaining
cellular
redox
homeostasis.
Disruption
this
finely
tuned
equilibrium
is
closely
linked
to
pathogenesis
wide
range
Recent
advances
have
broadened
our
understanding
molecular
mechanisms
underpinning
dysregulation,
highlighting
pivotal
roles
genomic
instability,
epigenetic
modifications,
protein
degradation,
metabolic
reprogramming.
findings
provide
foundation
for
exploring
regulation
mechanistic
basis
improving
therapeutic
strategies.
While
antioxidant-based
therapies
shown
early
promise
conditions
where
stress
plays
primary
pathological
role,
efficacy
diseases
characterized
complex,
multifactorial
etiologies
remains
controversial.
A
deeper,
context-specific
signaling,
particularly
redox-sensitive
proteins,
designing
targeted
aimed
at
re-establishing
balance.
Emerging
small
molecule
inhibitors
that
target
specific
cysteine
residues
proteins
demonstrated
promising
preclinical
outcomes,
setting
stage
forthcoming
clinical
trials.
In
review,
we
summarize
current
intricate
relationship
disease
also
discuss
how
these
insights
leveraged
optimize
strategies
practice.
Frontiers in Molecular Biosciences,
Journal Year:
2025,
Volume and Issue:
11
Published: Jan. 28, 2025
Aging
and
cancer
are
intricately
linked
through
shared
molecular
processes
that
influence
both
the
onset
of
malignancy
progression
age-related
decline.
As
organisms
age,
cellular
stress,
genomic
instability,
an
accumulation
senescent
cells
create
a
pro-inflammatory
environment
conducive
to
development.
Autophagy,
process
responsible
for
degrading
recycling
damaged
components,
plays
pivotal
role
in
this
relationship.
While
autophagy
acts
as
tumor-suppressive
mechanism
by
preventing
organelles
proteins,
often
exploit
it
survive
under
conditions
metabolic
stress
treatment
resistance.
The
interplay
between
aging,
cancer,
reveals
key
insights
into
tumorigenesis,
senescence,
proteostasis
dysfunction.
This
review
explores
connections
these
processes,
emphasizing
potential
autophagy-targeted
therapies
strategies
could
be
further
explored
aging
treatment.
Understanding
dual
roles
suppressing
promoting
offers
promising
avenues
therapeutic
interventions
aimed
at
improving
outcomes
elderly
patients
while
addressing
deterioration.
