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Pathologic role of glial nitric oxide in adult and pediatric neuroinflammatory diseases.
[x-linked adrenoleukodystrophy]
It
is
well
established
that
glial
cells
have
critical
roles
in
the
inflammatory
processes
in
the
central
nervous
system
(
CNS
)
.
These
cells
can
be
activated
by
a
variety
of
endogenous
and
exogenous
stimuli
(
i
.
e
.
gliosis
)
and
can
produce
high
levels
of
bioactive
compounds
that
are
noxious
for
neuronal
cell
function
.
One
of
the
most
important
molecules
released
by
activated
glial
cells
is
the
bioactive
free
radical
nitric
oxide
(
NO
)
.
Although
NO
physiologically
acts
as
both
neuromodulator
and
neurotransmitter
in
the
brain
,
excess
production
of
NO
by
glial
cells
has
diverse
harmful
effects
on
neuronal
function
,
causing
neuronal
cell
injury
/
death
.
The
production
of
NO
is
induced
by
overexpression
of
the
inducible
isoform
of
NO
synthase
(
iNOS
)
enzyme
in
glial
cells
.
In
this
review
,
we
describe
the
possible
mechanisms
that
underlie
the
iNOS-mediated
overproduction
of
glial
NO
in
several
pediatric
and
adult
neuropathologic
conditions
such
as
periventricular
leukomalacia
(
PVL
)
,
Krabbe
's
disease
,
X-
linked
adrenoleukodystrophy
(
ALD
)
and
multiple
sclerosis
(
MS
)
.
We
specifically
discuss
various
signaling
cascades
that
activate
several
transcription
factors
involved
in
the
iNOS
expression
in
both
astrocytes
and
microglia
.
We
also
discuss
the
consequences
of
iNOS-mediated
NO
production
in
neuroinflammatory
diseases
including
MS
.
A
complete
understanding
of
the
regulation
of
iNOS
expression
in
glial
cells
and
the
mechanisms
by
which
iNOS-mediated
NO
production
is
involved
in
neuroinflammation
can
provide
new
insights
into
the
identification
of
novel
targets
for
therapeutic
intervention
in
NO-mediated
neurologic
diseases
.
Diseases
Validation
Diseases presenting
"causing neuronal cell injury"
symptom
x-linked adrenoleukodystrophy
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