Targeting the Interplay Between Autophagy and the Nrf2 Pathway in Parkinson’s Disease with Potential Therapeutic Implications
Biomolecules,
Год журнала:
2025,
Номер
15(1), С. 149 - 149
Опубликована: Янв. 19, 2025
Parkinson’s
disease
(PD)
is
a
prevalent
neurodegenerative
disorder
marked
by
the
progressive
degeneration
of
midbrain
dopaminergic
neurons
and
resultant
locomotor
dysfunction.
Despite
over
two
centuries
recognition
as
chronic
disease,
exact
pathogenesis
PD
remains
elusive.
The
onset
progression
involve
multiple
complex
pathological
processes,
with
dysfunctional
autophagy
elevated
oxidative
stress
serving
critical
contributors.
Notably,
emerging
research
has
underscored
interplay
between
in
pathogenesis.
Given
limited
efficacy
therapies
targeting
either
dysfunction
or
stress,
it
crucial
to
elucidate
intricate
mechanisms
governing
their
develop
more
effective
therapeutics.
This
review
overviews
role
nuclear
factor
erythroid
2-related
2
(Nrf2),
pivotal
transcriptional
regulator
orchestrating
cellular
defense
against
these
processes.
By
elucidating
key
processes
PD,
this
will
deepen
our
comprehensive
understanding
multifaceted
underlying
may
uncover
potential
strategies
for
its
prevention
treatment.
Язык: Английский
Lactate Mediates Exercise-Induced Modulation of Mitophagy and Ferroptosis, Reducing Amyloid-Beta and Tau in Type 2 Diabetes: A Molecular Study
Опубликована: Янв. 1, 2025
Background:
This
study
examined
the
impact
of
lactate
accumulation,
induced
by
high-intensity
interval
training
(HIIT),
on
reducing
amyloid-beta
(Aβ)
and
tau
protein
levels
through
enhanced
mitophagy
decreased
ferroptosis
in
hippocampus
type
2
diabetic
rats.Methods:
Thirty-two
male
Wistar
rats
were
divided
into
four
groups:
control
(Co),
exercise
(EX),
diabetes
(DB),
with
(DB
+
EX).
Diabetes
was
DB
EX
groups
via
a
high-fat
diet
followed
streptozotocin
injection
(35
mg/kg).
The
performed
treadmill-based
HIIT,
involving
4–10
running
intervals
at
80–100%
Vmax.
Serum
hippocampal
expression
MCT2,
SIRT1,
BDNF,
p62,
Keap1,
NRF2,
MDA,
GPX4,
PINK1,
parkin,
Aβ,
Tau
assessed.Results:
In
group,
Parkin
elevated,
while
reduced
compared
to
group.Conclusion:
HIIT
enhances
reduces
lactate-SIRT1-BDNF
p62-Keap1-NRF2
pathways,
potentially
mitigating
Aβ
accumulation.
Язык: Английский
LncRNA TCONS_00067339 as a key regulatory factor inducing decreased cell viability and ferroptosis in neonatal hypoxic-ischemic brain damage
Brain Research,
Год журнала:
2025,
Номер
1854, С. 149562 - 149562
Опубликована: Март 8, 2025
Язык: Английский
Ferroptosis and hyperoxic lung injury: insights into pathophysiology and treatment approaches
Frontiers in Pharmacology,
Год журнала:
2025,
Номер
16
Опубликована: Март 18, 2025
Hyperoxia
therapy
is
a
critical
clinical
intervention
for
both
acute
and
chronic
illnesses.
However,
prolonged
exposure
to
high-concentration
oxygen
can
cause
lung
injury.
The
mechanisms
of
hyperoxic
injury
(HLI)
remain
incompletely
understood,
current
treatment
options
are
limited.
Improving
the
safety
hyperoxia
has
thus
become
an
urgent
priority.
Ferroptosis,
novel
form
regulated
cell
death
characterized
by
iron
accumulation
excessive
lipid
peroxidation,
been
implicated
in
pathogenesis
HLI,
including
diffuse
alveolar
damage,
vascular
endothelial
injury,
bronchopulmonary
dysplasia.
In
this
review,
we
analyze
latest
findings
on
ferroptosis
therapeutic
strategies
HLI.
Our
aim
provide
new
insights
HLI
facilitate
translation
these
from
bench
bedside.
Язык: Английский
Nebulized M2 macrophage-derived nanovesicles for the treatment of explosion-induced acute lung injury
Linqiang Tian,
Jie Jin,
Feng Lai
и другие.
Journal of Colloid and Interface Science,
Год журнала:
2025,
Номер
unknown, С. 137381 - 137381
Опубликована: Март 1, 2025
Язык: Английский
Complexin 2 contributes to the protective effect of NAD+ on neuronal survival following neonatal hypoxia-ischemia
Acta Pharmacologica Sinica,
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 17, 2025
Язык: Английский
The associations between brain aging and mitochondria dysfunction: Mechanism and intervention strategies
Deleted Journal,
Год журнала:
2025,
Номер
unknown, С. 1 - 16
Опубликована: Апрель 20, 2025
Brain
aging,
an
exquisitely
intricate
biological
phenomenon,
is
intertwined
with
cognitive
deterioration
and
the
pathogenesis
of
neurodegenerative
maladies.
Mitochondria,
cellular
powerhouses
responsible
for
energy
homeostasis,
assume
a
central
indispensable
role
in
this
process.
This
review
delves
deeply
into
multifaceted
associations
between
mitochondrial
dysfunction
brain
encompassing
perturbations
metabolism,
exacerbation
oxidative
stress,
aberrations
dynamics,
activation
inflammatory
response,
DNA
mutations,
all
which
interact
complex
network
to
drive
progression
aging.
Simultaneously,
it
undertakes
meticulous
dissection
functions
some
key
mitochondria-related
molecules
In
terms
intervention
strategies,
emerging
evidence
suggests
that
inhibition
cyclic
GMP-AMP
synthase-stimulator
interferon
genes
(cGAS-STING)
signaling
axis
holds
promise
alleviating
phenotypes
senescent
cells
tissues.
Downregulating
levels
relevant
transfer
RNA-derived
small
RNAs
(tsRNAs)
represents
potential
approach
safeguard
crucial
processes.
Supplementation
spermidine
spermine
has
demonstrated
efficacy
ameliorating
function
performance.
Moreover,
comprehensive
paradigms
targeting
antioxidative
stress
responses,
autophagy
regulation
offer
avenues
retarding
Collectively,
existing
body
research
furnishes
profound
insights
underlying
mechanisms
aging
serves
as
bedrock
development
efficacious
modalities.
Future
imperatives
should
center
on
elucidating
molecular
mechanisms,
formulating
highly
precise
expediting
translation
basic
findings
clinical
applications.
utmost
significance
enhancing
quality
life
elderly
forestalling
onset
diseases.
Язык: Английский
Nuclear factor erythroid 2-related factor-mediated signaling alleviates ferroptosis during cerebral ischemia-reperfusion injury
Biomedicine & Pharmacotherapy,
Год журнала:
2024,
Номер
180, С. 117513 - 117513
Опубликована: Сен. 27, 2024
Язык: Английский
Sex and Region-Specific Disruption of Autophagy and Mitophagy in Alzheimer's Disease: Linking Cellular Dysfunction to Cognitive Decline
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Окт. 31, 2024
Abstract
Macroautophagy
and
mitophagy
are
critical
processes
in
Alzheimer’s
disease
(AD),
yet
their
links
to
behavioral
outcomes,
particularly
sex-specific
differences,
not
fully
understood.
This
study
investigates
autophagy
(LC3B-II,
SQSTM1)
(BNIP3L,
BNIP3,
BCL2L13)
markers
the
cortex
hippocampus
of
male
female
3xTg-AD
mice,
using
western
blotting,
transmission
electron
microscopy
(TEM),
tests
(novel
object
recognition
novel
placement).
Significant
differences
emerged:
mice
exhibited
autophagosome
accumulation
due
impaired
degradation
cortex,
while
males
showed
fewer
autophagosomes,
especially
hippocampus,
without
significant
changes.
TEM
analyses
demonstrated
variations
mitochondrial
mitophagosome
numbers
correlated
with
memory
outcomes.
Females
had
enhanced
mitophagy,
higher
BNIP3L
BCL2L13
levels,
whereas
elevated
BNIP3
dimers.
Cognitive
deficits
females
dysfunction
males,
LC3B-II
levels
associated
positively
cognitive
performance,
suggesting
protective
effects.
Using
machine
learning,
we
predicted
based
on
data,
pioneering
a
predictive
approach
cellular
outcomes
AD.
These
findings
underscore
importance
regulation
AD
support
personalized
therapeutic
approaches
targeting
these
pathways.
Integrating
learning
emphasizes
its
potential
advance
neurodegenerative
research.
Figure
Graphical
Sex-specific
(AD)
highlighted.
Female
show
deficits,
exhibit
behavior.
Язык: Английский