Frontiers in Immunology,
Journal Year:
2022,
Volume and Issue:
13
Published: Feb. 25, 2022
Stroke
is
the
second
leading
cause
of
global
death
and
characterized
by
high
rates
mortality
disability.
Oxidative
stress
accompanied
other
pathological
processes
that
together
lead
to
secondary
brain
damage
in
stroke.
As
major
component
brain,
glial
cells
play
an
important
role
normal
development
injury
processes.
Multiple
connections
exist
pathophysiological
changes
reactive
oxygen
species
(ROS)
metabolism
glia
cell
activation.
Astrocytes
microglia
are
rapidly
activated
after
stroke,
generating
large
amounts
ROS
via
mitochondrial
NADPH
oxidase
pathways,
causing
oxidative
themselves
neurons.
Meanwhile,
alterations
morphology
function,
mediate
their
processes,
such
as
neuroinflammation,
excitotoxicity,
blood-brain
barrier
damage.
In
contrast,
protect
Central
Nervous
System
(CNS)
from
synthesizing
antioxidants
regulating
Nuclear
factor
E2-related
2
(Nrf2)
pathway,
among
others.
Although
numerous
previous
studies
have
focused
on
immune
function
cells,
little
attention
has
been
paid
stress.
this
paper,
we
discuss
adverse
consequences
production
oxidative-antioxidant
imbalance
addition,
further
describe
biological
potential
therapeutic
tools
based
cells.
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
23(11), P. 6224 - 6224
Published: June 2, 2022
Vascular
cognitive
impairment
and
dementia
(VCID)
is
a
major
heterogeneous
brain
disease
caused
by
multiple
factors,
it
the
second
most
common
type
of
in
world.
It
long-term
chronic
low
perfusion
whole
or
local
area,
eventually
develops
into
severe
dysfunction
syndrome.
Because
disease's
ambiguous
classification
diagnostic
criteria,
there
no
clear
treatment
strategy
for
VCID,
association
between
cerebrovascular
pathology
controversial.
Neuroinflammation
an
immunological
cascade
reaction
mediated
glial
cells
central
nervous
system
where
innate
immunity
resides.
Inflammatory
reactions
could
be
triggered
various
damaging
events,
including
hypoxia,
ischemia,
infection.
Long-term
hypoperfusion-induced
ischemia
hypoxia
can
overactivate
neuroinflammation,
causing
apoptosis,
blood-brain
barrier
damage
other
pathological
changes,
triggering
aggravating
occurrence
development
VCID.
In
this
review,
we
will
explore
mechanisms
neuroinflammation
induced
hypoperfusion
emphasize
important
role
VCID
from
perspective
immune
cells,
mediators
signaling
pathways,
so
as
to
provide
valuable
ideas
prevention
disease.
Frontiers in Immunology,
Journal Year:
2022,
Volume and Issue:
13
Published: Feb. 25, 2022
Stroke
is
the
second
leading
cause
of
global
death
and
characterized
by
high
rates
mortality
disability.
Oxidative
stress
accompanied
other
pathological
processes
that
together
lead
to
secondary
brain
damage
in
stroke.
As
major
component
brain,
glial
cells
play
an
important
role
normal
development
injury
processes.
Multiple
connections
exist
pathophysiological
changes
reactive
oxygen
species
(ROS)
metabolism
glia
cell
activation.
Astrocytes
microglia
are
rapidly
activated
after
stroke,
generating
large
amounts
ROS
via
mitochondrial
NADPH
oxidase
pathways,
causing
oxidative
themselves
neurons.
Meanwhile,
alterations
morphology
function,
mediate
their
processes,
such
as
neuroinflammation,
excitotoxicity,
blood-brain
barrier
damage.
In
contrast,
protect
Central
Nervous
System
(CNS)
from
synthesizing
antioxidants
regulating
Nuclear
factor
E2-related
2
(Nrf2)
pathway,
among
others.
Although
numerous
previous
studies
have
focused
on
immune
function
cells,
little
attention
has
been
paid
stress.
this
paper,
we
discuss
adverse
consequences
production
oxidative-antioxidant
imbalance
addition,
further
describe
biological
potential
therapeutic
tools
based
cells.
