Cellular and Molecular Neurobiology,
Год журнала:
2023,
Номер
43(7), С. 3137 - 3160
Опубликована: Июнь 28, 2023
Abstract
Translation
of
neuroprotective
treatment
effects
from
experimental
animal
models
to
patients
with
cerebral
ischemia
has
been
challenging.
Since
pathophysiological
processes
may
vary
across
species,
an
model
clarify
human-specific
neuronal
pathomechanisms
help.
We
conducted
a
scoping
review
the
literature
on
human
in
vitro
that
have
used
study
responses
or
hypoxia,
parts
cascade
investigated
those
models,
and
evidence
interventions.
included
147
studies
four
different
models.
The
majority
(132/147)
was
SH-SY5Y
cells,
which
is
cancerous
cell
line
derived
single
neuroblastoma
patient.
Of
these,
119/132
undifferentiated
lack
many
characteristics.
Two
healthy
induced
pluripotent
stem
networks.
Most
microscopic
measures
established
hypoxia
death,
oxidative
stress,
inflammation.
Only
one
effect
network
functionality
using
micro-electrode
arrays.
Treatment
targets
inflammation,
stimulation.
discuss
(dis)advantages
various
systems
propose
future
perspectives
for
research
into
hypoxia.
Graphical
International Journal of Molecular Sciences,
Год журнала:
2022,
Номер
23(5), С. 2814 - 2814
Опубликована: Март 4, 2022
In
this
review,
we
provide
recent
data
on
the
role
of
mTOR
kinase
in
brain
under
physiological
conditions
and
after
damage,
with
a
particular
focus
cerebral
ischemia.
We
cover
upstream
downstream
pathways
that
regulate
activation
state
complexes.
Furthermore,
summarize
advances
our
understanding
mTORC1
mTORC2
status
ischemia–hypoxia
at
tissue
cellular
levels
analyze
existing
evidence
related
to
two
types
neural
cells,
namely
glia
neurons.
Finally,
discuss
potential
use
as
therapeutic
targets
stroke.
Oxidative Medicine and Cellular Longevity,
Год журнала:
2022,
Номер
2022, С. 1 - 15
Опубликована: Июнь 8, 2022
Stroke
is
one
of
the
leading
causes
death
and
disability
worldwide.
Autophagy
a
conserved
cellular
catabolic
pathway
that
maintains
homeostasis
by
removal
damaged
proteins
organelles,
which
critical
for
maintenance
energy
function
cells.
Accumulating
evidence
demonstrates
autophagy
plays
important
roles
in
pathophysiological
mechanisms
under
ischemic
stroke.
Previous
investigations
show
serves
as
"double-edged
sword"
stroke
it
can
either
promote
survival
neuronal
cells
or
induce
cell
special
conditions.
Following
stroke,
activated
inhibited
several
types
brain,
including
neurons,
astrocytes,
microglia,
well
microvascular
endothelial
cells,
involves
inflammatory
activation,
modulation
microglial
phenotypes,
blood-brain
barrier
permeability.
However,
exact
underlying
role
are
not
fully
understood.
This
review
focuses
on
recent
advances
regarding
potential
molecular
different
types.
The
focus
also
discussing
effect
its
possible
mechanisms.
In
addition,
therapeutic
strategies
targeting
reviewed.
Frontiers in Pharmacology,
Год журнала:
2022,
Номер
13
Опубликована: Сен. 6, 2022
Stroke
remains
one
of
the
leading
reasons
mortality
and
physical
disability
worldwide.
The
treatment
cerebral
ischemic
stroke
faces
challenges,
partly
due
to
a
lack
effective
treatments.
In
this
study,
we
demonstrated
that
autophagy
was
stimulated
by
transient
middle
artery
occlusion/reperfusion
(MCAO/R)
oxygen-glucose
deprivation/reoxygenation
(OGD/R).
Treatment
with
(−)-epigallocatechin-3-gallate
(EGCG),
bioactive
ingredient
in
green
tea,
able
mitigate
ischemia/reperfusion
injury
(CIRI),
given
evidence
EGCG
administration
could
reduce
infarct
volume
protect
poststroke
neuronal
loss
MCAO/R
mice
vivo
attenuate
cell
OGD/R-challenged
HT22
cells
vitro
through
suppressing
activity.
Mechanistically,
inhibited
via
modulating
AKT/AMPK/mTOR
phosphorylation
pathway
both
models
stroke,
which
further
confirmed
results
GSK690693,
an
AKT/AMPK
inhibitor,
rapamycin,
inhibitor
mTOR,
reversed
aforementioned
changes
signaling
pathway.
Overall,
application
relieved
CIRI
Frontiers in Neurology,
Год журнала:
2022,
Номер
13
Опубликована: Авг. 30, 2022
Ischemic
stroke
is
a
highly
disabling
and
potentially
fatal
disease.
After
ischemic
stroke,
autophagy
plays
key
regulatory
role
as
an
intracellular
catabolic
pathway
for
misfolded
proteins
damaged
organelles.
Mounting
evidence
indicates
that
astrocytes
are
strongly
linked
to
the
occurrence
development
of
cerebral
ischemia.
In
recent
years,
great
progress
has
been
made
in
investigation
astrocyte
during
stroke.
This
article
summarizes
roles
potential
mechanisms
briefly
expounds
on
crosstalk
with
pathological
its
protective
effect
neurons,
reviews
astrocytic
autophagy-targeted
therapeutic
methods
The
broader
aim
report
provide
new
perspectives
strategies
treatment
ischemia
reference
future
research
International Journal of Molecular Sciences,
Год журнала:
2023,
Номер
24(18), С. 13793 - 13793
Опубликована: Сен. 7, 2023
Autophagy
is
a
self-defense
and
self-degrading
intracellular
system
involved
in
the
recycling
elimination
of
payload
cytoplasmic
redundant
components,
aggregated
or
misfolded
proteins
pathogens
to
maintain
cell
homeostasis
physiological
function.
activated
response
metabolic
stress
starvation
cells
by
updating
organelles
dysfunctional
proteins.
In
neurodegenerative
diseases,
such
as
cerebral
ischemia,
autophagy
disturbed,
e.g.,
result
pathological
accumulation
associated
with
Alzheimer’s
disease
their
structural
changes.
Postischemic
brain
neurodegeneration,
disease,
characterized
amyloid
tau
protein.
After
was
found
be
neuronal,
glial
vascular
cells.
Some
studies
have
shown
protective
properties
postischemic
brain,
while
other
completely
opposite
properties.
Thus,
now
presented
double-edged
sword
possible
therapeutic
potential
ischemia.
The
exact
role
regulatory
pathways
that
are
ischemia
not
been
conclusively
elucidated.
This
review
aims
provide
comprehensive
look
at
advances
study
behavior
for
ischemic
injury.
addition,
importance
neurodegeneration
after
has
highlighted.
also
presents
possibility
modulating
machinery
through
various
compounds
on
development
