Life,
Год журнала:
2023,
Номер
13(4), С. 970 - 970
Опубликована: Апрель 8, 2023
Alzheimer’s
disease
(AD),
a
progressive
and
chronic
neurodegenerative
syndrome,
is
categorized
by
cognitive
memory
damage
caused
the
aggregations
of
abnormal
proteins,
specifically
including
Tau
proteins
β-amyloid
in
brain
tissue.
Moreover,
mitochondrial
dysfunctions
are
principal
causes
AD,
which
associated
with
mitophagy
impairment.
Investigations
exploring
pharmacological
therapies
alongside
AD
have
explicitly
concentrated
on
molecules
accomplished
preventing/abolishing
gatherings
abovementioned
mitochondria
damages.
Mitophagy
removal
dead
autophagy
process.
Damages
mitophagy,
manner
diversified
degeneracy
resulting
an
ongoing
aggregation
malfunctioning
mitochondria,
were
also
suggested
to
support
AD.
Recently,
plentiful
reports
link
between
defective
This
treaty
highlights
updated
outlines
modern
innovations
developments
machinery
brains.
therapeutic
nanotherapeutic
strategies
targeting
dysfunction
presented
this
review.
Based
significant
role
diminished
we
suggest
that
application
different
approaches
aimed
at
stimulating
would
be
beneficial
for
or
reducing
induced
International Journal of Molecular Sciences,
Год журнала:
2023,
Номер
24(6), С. 5896 - 5896
Опубликована: Март 20, 2023
Mitochondrial
dysfunction
is
considered
an
early
event
of
Alzheimer
disease
(AD).
D-ribose
a
natural
monosaccharide
that
exists
in
cells,
especially
mitochondria,
and
can
lead
to
cognitive
dysfunction.
However,
the
reason
for
this
unclear.
Berberine
(BBR)
isoquinoline
alkaloid
target
mitochondria
has
great
prospect
treatment
AD.
The
methylation
PINK1
reinforces
burden
Alzheimer’s
pathology.
This
study
explores
role
BBR
mitophagy
function
AD
related
DNA
methylation.
APP/PS1
mice
N2a
cells
were
treated
with
D-ribose,
BBR,
inhibitor
Mdivi-1
observe
their
effects
on
mitochondrial
morphology,
mitophagy,
neuron
histology,
pathology,
animal
behavior,
results
showed
induced
dysfunction,
damage,
impairment.
inhibition
promoter
reverse
above
caused
by
improve
function,
restore
through
PINK1–Parkin
pathway,
thus
reducing
deficits
experiment
puts
new
light
mechanism
action
impairment
reveals
insights
use
treatment.
Clinical Epigenetics,
Год журнала:
2024,
Номер
16(1)
Опубликована: Янв. 3, 2024
Abstract
Background
The
management
of
myocardial
ischemia–reperfusion
injury
(MIRI)
presents
continuous
therapeutic
challenges.
NAD-dependent
deacetylase
Sirtuin
6
(Sirt6)
plays
distinct
roles
in
various
disease
contexts
and
is
hence
investigated
for
potential
applications
MIRI.
This
study
aimed
to
examine
the
impact
Sirt6-overexpressing
exosomes
derived
from
adipose
stem
cells
(S-ASC-Exo)
on
MIRI,
focusing
their
influence
AIM2-pyroptosis
mitophagy
processes.
sirtuin
family
proteins,
particularly
(Sirt6),
play
a
pivotal
role
these
explore
effects
Sirt6-enriched
regulating
Results
Bioinformatic
analysis
revealed
significant
downregulation
Sirt6
MIRI
subjected
control
group,
causing
consequential
increase
pyroptosis
regulator
expressions.
Therefore,
our
that
influenced
progression
through
regulation
target
proteins
AIM2
GSDMD,
associated
with
pyroptosis,
p62
Beclin-1,
related
mitophagy.
introduction
S-ASC-Exo
inhibited
while
enhancing
Consequently,
this
led
reduction
GSDMD
cleavage
endothelial
cells,
catalyzing
deceleration
atherosclerosis.
Extensive
vivo
vitro
assays
were
performed
validate
expressions
specific
genes
which
affirmed
dynamic
modulation
by
exosomes.
Furthermore,
treatment
drastically
ameliorated
cardiac
functions
limited
infarct
size,
underlining
cardioprotective
attributes.
Conclusions
Our
underscores
managing
We
demonstrated
profound
effect,
evident
enhanced
function
attenuated
tissue
damage,
strategic
Given
intricate
interplay
between
aforementioned
processes,
comprehensive
understanding
pathways
essential
fully
exploit
Sirt6.
Altogether,
findings
indicate
promise
as
novel
strategy
treating
injuries
cardiovascular
diseases
at
large.
Future
research
needs
underscore
optimizing
balance
during
ischemia
avoid
loss
normal
myocytes.
Journal of Chemical Information and Modeling,
Год журнала:
2024,
Номер
64(5), С. 1502 - 1511
Опубликована: Фев. 27, 2024
Protein
function
prediction
is
essential
for
disease
treatment
and
drug
development;
yet,
traditional
biological
experimental
methods
are
less
efficient
in
annotating
protein
function,
existing
automated
fail
to
fully
leverage
multisource
data.
Here,
we
present
MSF-PFP,
a
computational
framework
that
fuses
data
features
predict
with
high
accuracy.
Our
designs
specific
models
feature
extraction
based
on
the
characteristics
of
various
sources,
including
global-local-individual
strategy
local
location
features.
MSF-PFP
then
integrates
extracted
through
fusion
model,
ultimately
categorizing
functions.
Experimental
results
demonstrate
outperforms
eight
state-of-the-art
models,
achieving
FMax
scores
0.542,
0.675,
0.624
process
(BP),
molecular
(MF),
cellular
component
(CC),
respectively.
The
source
code
set
available
at
https://swanhub.co/TianGua/MSF-PFP,
facilitating
further
exploration
validation
proposed
framework.
This
study
highlights
potential
enhancing
prediction,
contributing
improved
therapy
medication
discovery
strategies.
Translational Psychiatry,
Год журнала:
2024,
Номер
14(1)
Опубликована: Июнь 10, 2024
The
etiopathogenesis
of
late-onset
Alzheimer's
disease
(AD)
is
increasingly
recognized
as
the
result
combination
aging
process,
toxic
proteins,
brain
dysmetabolism,
and
genetic
risks.
Although
role
mitochondrial
dysfunction
in
pathogenesis
AD
has
been
well-appreciated,
interaction
between
function
variability
promoting
dementia
still
poorly
understood.
In
this
study,
by
tissue-specific
transcriptome-wide
association
study
(TWAS)
further
meta-analysis,
we
examined
solute
carrier
family
(SLC25)
genes
three
independent
cohorts
identified
AD-susceptibility
genes,
including
SLC25A10,
SLC25A17,
SLC25A22.
Integrative
analysis
using
neuroimaging
data
hippocampal
TWAS-predicted
gene
expression
susceptibility
showed
an
inverse
correlation
SLC25A22
with
atrophy
rate
patients,
which
outweighed
impacts
sex,
age,
apolipoprotein
E4
(ApoE4).
Furthermore,
downregulation
demonstrated
onset,
compared
other
two
significant
genes.
Pathway
network
related
to
defects
neuronal
development,
echoing
enrichment
human
glutamatergic
neurons.
most
parsimonious
interpretation
results
that
have
SLC25
through
prediction
expression.
Moreover,
our
findings
mechanistically
yield
insight
into
cascade
hypothesis
pave
way
for
future
development
diagnostic
tools
early
prevention
from
a
perspective
precision
medicine
targeting
mitochondria-related
