Biology,
Год журнала:
2024,
Номер
13(9), С. 719 - 719
Опубликована: Сен. 12, 2024
Neurodegenerative
diseases
(NDs),
like
amyotrophic
lateral
sclerosis
(ALS),
Alzheimer's
disease
(AD),
and
Parkinson's
(PD),
primarily
affect
the
central
nervous
system,
leading
to
progressive
neuronal
loss
motor
cognitive
dysfunction.
However,
recent
studies
have
revealed
that
muscle
tissue
also
plays
a
significant
role
in
these
diseases.
ALS
is
characterized
by
severe
wasting
as
result
of
neuron
degeneration,
well
alterations
gene
expression,
protein
aggregation,
oxidative
stress.
Muscle
atrophy
mitochondrial
dysfunction
are
observed
AD,
which
may
exacerbate
decline
due
systemic
metabolic
dysregulation.
PD
patients
exhibit
fiber
atrophy,
altered
composition,
α-synuclein
aggregation
within
cells,
contributing
symptoms
progression.
Systemic
inflammation
impaired
degradation
pathways
common
among
disorders,
highlighting
key
player
Understanding
muscle-related
changes
offers
potential
therapeutic
avenues,
such
targeting
function,
reducing
inflammation,
promoting
regeneration
with
exercise
pharmacological
interventions.
This
review
emphasizes
importance
considering
an
integrative
approach
neurodegenerative
research,
both
peripheral
pathological
mechanisms,
order
develop
more
effective
treatments
improve
patient
outcomes.
Ubiquitination
is
an
enzymatic
process
characterized
by
the
covalent
attachment
of
ubiquitin
to
target
proteins,
thereby
modulating
their
degradation,
transportation,
and
signal
transduction.
By
precisely
regulating
protein
quality
quantity,
ubiquitination
essential
for
maintaining
homeostasis,
DNA
repair,
cell
cycle
regulation,
immune
responses.
Nevertheless,
diversity
enzymes
extensive
involvement
in
numerous
biological
processes
contribute
complexity
variety
diseases
resulting
from
dysregulation.
The
relies
on
a
sophisticated
system,
domains,
receptors,
which
collectively
impart
versatility
pathway.
widespread
presence
highlights
its
potential
induce
pathological
conditions.
Ubiquitinated
proteins
are
predominantly
degraded
through
proteasomal
also
plays
key
role
localization
transport,
as
well
inflammatory
pathways.
This
review
systematically
delineates
roles
genomic
stability,
cellular
proliferation,
Furthermore,
mechanisms
implicated
various
pathologies,
alongside
current
modulators
discussed.
Enhancing
our
comprehension
aims
provide
novel
insights
into
involving
propose
innovative
therapeutic
strategies
clinical
Biomolecules,
Год журнала:
2024,
Номер
14(6), С. 673 - 673
Опубликована: Июнь 8, 2024
One
of
the
biggest
problems
in
treatment
idiopathic
Parkinson’s
disease
is
lack
new
drugs
that
slow
its
progression.
L-Dopa
remains
star
drug
this
disease,
although
it
induces
severe
side
effects.
The
failure
clinical
studies
with
depends
on
use
preclinical
models
based
neurotoxins
do
not
represent
what
happens
since
they
induce
rapid
and
expansive
neurodegeneration.
We
have
recently
proposed
a
single-neuron
degeneration
model
for
requires
years
to
accumulate
enough
lost
neurons
onset
motor
symptoms.
This
excessive
formation
aminochrome
during
neuromelanin
synthesis
surpass
neuroprotective
action
enzymes
DT-diaphorase
glutathione
transferase
M2-2,
which
prevent
neurotoxic
effects
aminochrome.
Although
an
effect,
stereotaxic
injection
endogenous
neurotoxin
cannot
be
used
generate
animal.
Therefore,
aim
review
evaluate
strategies
pharmacologically
increasing
expression
DT
diaphorase
GSTM2-2
molecules
vesicular
monoamine
transporter
2,
such
as
pramipexole.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(3), С. 1641 - 1641
Опубликована: Янв. 29, 2024
Parkinson’s
disease
(PD)
is
a
common
neurodegenerative
disorder
with
complicated
etiology
and
pathogenesis.
α-Synuclein
aggregation,
dopaminergic
(DA)
neuron
loss,
mitochondrial
injury,
oxidative
stress,
inflammation
are
involved
in
the
process
of
PD.
Neuroinflammation
has
been
recognized
as
key
element
initiation
progression
In
this
review,
we
summarize
inflammatory
response
pathogenic
mechanisms
Additionally,
describe
potential
anti-inflammatory
therapies,
including
nod-like
receptor
pyrin
domain
containing
protein
3
(NLRP3)
inflammasome
inhibition,
nuclear
factor
κB
(NF-κB)
microglia
astrocyte
nicotinamide
adenine
dinucleotide
phosphate
(NADPH)
oxidase
peroxisome
proliferator-activated
γ
(PPARγ)
agonist,
targeting
mitogen-activated
kinase
(MAPK)
pathway,
adenosine
monophosphate-activated
(AMPK)-dependent
α-synuclein,
miRNA,
acupuncture,
exercise.
The
review
focuses
on
will
help
designing
new
prevention
strategies
for
Scientific Reports,
Год журнала:
2025,
Номер
15(1)
Опубликована: Янв. 21, 2025
Aging
is
characterized
by
cellular
degeneration
and
impaired
physiological
functions,
leading
to
a
decline
in
male
sexual
desire
reproductive
capacity.
Oxidative
stress
(OS)
lead
testicular
aging
impairing
the
system,
but
potential
mechanisms
remain
unclear.
In
present
study,
functional
status
of
tissues
from
young
aged
boars
was
compared,
transcriptional
responses
Leydig
cells
(LCs)
hydrogen
peroxide
(H2O2)-induced
senescence
were
explored,
revealing
role
OS
promoting
system.
601
differentially
expressed
genes
(DEGs)
associated
with
OS,
cell
cycle
regulation,
intracellular
processes
identified.
These
DEGs
significantly
enriched
critical
pathways,
including
p53
signaling
pathway,
autophagy,
senescence.
Protein-protein
interaction
(PPI)
network
analysis
unveiled
15
key
related
DNA
replication,
polo-like
kinase
3
(PLK3)
exhibiting
increased
expression
under
OS.
vitro,
PLK3
knockdown
enhanced
viability
antioxidant
capacity
LCs
This
study
deepens
our
understanding
how
respond
provides
new
therapeutic
targets
for
enhancing
resistance
oxidative
damage
tissue
health.
Biomolecules,
Год журнала:
2025,
Номер
15(3), С. 349 - 349
Опубликована: Фев. 28, 2025
The
ubiquitin–proteasome
system
(UPS)
and
autophagy
maintain
protein
homeostasis,
which
is
critical
to
cellular
function
survival.
dysregulation
of
these
pathways
has
been
recognized
as
a
hallmark
acute
kidney
injury
chronic
disease.
This
review
elucidates
the
role
UPS
in
disease,
namely
through
inflammation,
oxidative
stress,
fibrosis
apoptosis.
NF-κB,
TGF-β
mitochondrial
failure
result
glomerular
tubulointerstitial
due
impaired
proteostasis
podocytes
tubular
epithelial
cells.
Recent
studies
have
revealed
connection
between
autophagic
process
UPS,
wherein
compensatory
mechanisms
aim
spike
down
proteotoxic
stress
but
eventually
seem
inadequate
cases
derangement.
Low-dose
pharmacological
inhibitors,
modulators,
new
gene
nanotechnology-based
treatments
may
all
help
restore
balance
reduce
injury.
A
more
thorough
understanding
needed
develop
kidney-protective
disease-modifying
therapeutic
interventions.
