Cells,
Journal Year:
2025,
Volume and Issue:
14(7), P. 511 - 511
Published: March 29, 2025
Oxidative
stress
(OS)
is
an
established
hallmark
of
cancer
and
neurodegenerative
disorders
(NDDs),
which
contributes
to
genomic
instability
neuronal
loss.
This
review
explores
the
contrasting
role
OS
in
stem
cells
(CSCs)
NDDs.
Elevated
levels
reactive
oxygen
species
(ROS)
contribute
promote
tumor
initiation
progression
CSCs,
while
NDDs
such
as
Alzheimer’s
Parkinson’s
disease,
accelerates
death
impairs
cellular
repair
mechanisms.
Both
scenarios
involve
disruption
delicate
balance
between
pro-oxidant
antioxidant
systems,
leads
chronic
oxidative
stress.
Notably,
CSCs
neurons
display
alterations
redox-sensitive
signaling
pathways,
including
Nrf2
NF-κB,
influence
cell
survival,
proliferation,
differentiation.
Mitochondrial
dynamics
further
illustrate
these
differences:
enhanced
function
supports
adaptability
whereas
impairments
heighten
vulnerability.
Understanding
common
mechanisms
OS-induced
redox
imbalance
may
provide
insights
for
developing
interventions,
addressing
aging
hallmarks,
potentially
mitigating
or
preventing
both
NeuroMolecular Medicine,
Journal Year:
2025,
Volume and Issue:
27(1)
Published: March 3, 2025
Abstract
Alzheimer’s
disease
(AD)
and
atherosclerosis
(AS)
are
two
chronic
diseases
with
seemingly
distinct
pathologies.
However,
emerging
research
points
to
a
bidirectional
relationship
driven
by
common
mechanisms,
such
as
inflammation,
oxidative
stress,
dysregulation
of
Amyloid-Beta
(Aβ).
This
review
focuses
on
the
role
Aβ
critical
molecular
link
between
AD
AS,
emphasizing
its
contribution
neuronal
impairment
vascular
damage.
Specifically,
peripheral
produced
in
pancreas
skeletal
muscle
tissues
exacerbates
AS
promoting
endothelial
dysfunction
insulin
resistance
(IR).
Furthermore,
accelerates
progression
impairing
cerebral
blood
flow
inducing
hypoxia,
causing
accumulation.
critically
evaluates
recent
findings,
highlighting
inconsistencies
clinical
studies
suggesting
future
directions.
Understanding
influence
could
pave
way
for
novel
therapeutic
approaches
targeting
shared
pathways,
particularly
clearance
inflammation.
Cells,
Journal Year:
2025,
Volume and Issue:
14(7), P. 511 - 511
Published: March 29, 2025
Oxidative
stress
(OS)
is
an
established
hallmark
of
cancer
and
neurodegenerative
disorders
(NDDs),
which
contributes
to
genomic
instability
neuronal
loss.
This
review
explores
the
contrasting
role
OS
in
stem
cells
(CSCs)
NDDs.
Elevated
levels
reactive
oxygen
species
(ROS)
contribute
promote
tumor
initiation
progression
CSCs,
while
NDDs
such
as
Alzheimer’s
Parkinson’s
disease,
accelerates
death
impairs
cellular
repair
mechanisms.
Both
scenarios
involve
disruption
delicate
balance
between
pro-oxidant
antioxidant
systems,
leads
chronic
oxidative
stress.
Notably,
CSCs
neurons
display
alterations
redox-sensitive
signaling
pathways,
including
Nrf2
NF-κB,
influence
cell
survival,
proliferation,
differentiation.
Mitochondrial
dynamics
further
illustrate
these
differences:
enhanced
function
supports
adaptability
whereas
impairments
heighten
vulnerability.
Understanding
common
mechanisms
OS-induced
redox
imbalance
may
provide
insights
for
developing
interventions,
addressing
aging
hallmarks,
potentially
mitigating
or
preventing
both