Frontiers in Cell and Developmental Biology,
Journal Year:
2021,
Volume and Issue:
9
Published: Jan. 28, 2021
Brain
disorders
include
neurodegenerative
diseases
(NDs)
with
different
conditions
that
primarily
affect
the
neurons
and
glia
in
brain.
However,
risk
factors
pathophysiological
mechanisms
of
NDs
have
not
been
fully
elucidated.
Homeostasis
intracellular
Ca
2+
concentration
pH
(pH
i
)
is
crucial
for
cell
function.
The
regulatory
processes
these
ionic
may
be
absent
or
excessive
pathological
conditions,
leading
to
a
loss
death
distinct
regions
ND
patients.
Herein,
we
review
potential
involvement
transient
receptor
(TRP)
channels
NDs,
where
disrupted
homeostasis
leads
death.
capability
TRP
restore
excite
through
regulation
depending
on
level
plasma
membrane
ATPase
(PMCA)
activity
discussed
detail.
As
PMCA
simultaneously
affects
as
well
,
thus
play
vital
roles
modulating
various
types
specific
brain
are
expressed.
For
this
reason,
dysfunction
and/or
under
disrupts
neuronal
due
abnormal
levels
brain,
resulting
NDs.
This
addresses
function
controlling
pH,
which
provide
novel
targets
treating
Frontiers in Cellular Neuroscience,
Journal Year:
2021,
Volume and Issue:
15
Published: April 9, 2021
The
voltage-gated
proton
channel
Hv1
is
a
newly
discovered
ion
that
highly
conserved
among
species.
It
known
not
only
expressed
in
peripheral
immune
cells
but
also
one
of
the
major
channels
tissue-resident
microglia
central
nervous
systems
(CNS).
One
key
role
for
its
interaction
with
NADPH
oxidase
2
(NOX2)
to
regulate
reactive
oxygen
species
(ROS)
and
cytosolic
pH.
Emerging
data
suggest
excessive
ROS
production
increases
requires
currents
through
injured
CNS,
manipulations
ablate
expression
or
induce
loss
function
may
provide
neuroprotection
CNS
injury
models
including
stroke,
traumatic
brain
injury,
spinal
cord
injury.
Recent
demonstrating
microglial
Hv1-mediated
signaling
pathophysiology
further
supports
idea
as
mechanism
posttraumatic
neuroinflammation
neurodegeneration.
In
this
review,
we
summarize
main
findings
Hv1,
pattern,
cellular
mechanism,
aging,
animal
disease
pathology.
We
discuss
potential
therapeutic
target
FEBS Open Bio,
Journal Year:
2023,
Volume and Issue:
13(11), P. 2020 - 2034
Published: Aug. 22, 2023
Neuropathic
pain
(NP),
resulting
from
nerve
injury,
alters
neural
plasticity
in
spinal
cord
and
brain
via
the
release
of
inflammatory
mediators.
The
remodeling
store-operated
calcium
entry
(SOCE)
involves
refilling
endoplasmic
reticulum
STIM1
Orai1
proteins
is
crucial
for
maintaining
neurotransmitter
release.
mechanism
underlying
SOCE-mediated
NP
remains
largely
unknown.
In
this
study,
we
found
was
significantly
higher
during
neuropathic
pain,
major
component
specifically
co-localized
with
neuronal
markers.
Intrathecal
injection
SOCE
antagonist
SKF96365
remarkably
alleviated
injury-
formalin-induced
suppressed
c-Fos
expression
response
to
innocuous
mechanical
stimulation.
RNA
sequencing
revealed
that
altered
transcription
factors,
including
Fos,
Junb,
Socs3,
pain.
order
identify
genes
critical
SKF96365-induced
effects,
performed
weighted
gene
co-expression
network
analysis
(WGCNA)
most
correlated
paw
withdrawal
latency
phenotypes.
Of
16
modules,
MEsalmon
module
highly
induced
effects.
Kyoto
Encyclopedia
Genes
Genomes
(KEGG)
showed
enriched
were
related
Toll-like
receptor
signaling,
steroid
biosynthesis,
chemokine
which
may
mediate
analgesic
effect
caused
by
SKF9636
treatment.
Additionally,
YM-58483
produced
similar
effects
Our
results
suggest
manipulation
signaling
might
be
a
promising
target
relief
regulating
production
factor
expression.
Frontiers in Cell and Developmental Biology,
Journal Year:
2021,
Volume and Issue:
9
Published: Jan. 28, 2021
Brain
disorders
include
neurodegenerative
diseases
(NDs)
with
different
conditions
that
primarily
affect
the
neurons
and
glia
in
brain.
However,
risk
factors
pathophysiological
mechanisms
of
NDs
have
not
been
fully
elucidated.
Homeostasis
intracellular
Ca
2+
concentration
pH
(pH
i
)
is
crucial
for
cell
function.
The
regulatory
processes
these
ionic
may
be
absent
or
excessive
pathological
conditions,
leading
to
a
loss
death
distinct
regions
ND
patients.
Herein,
we
review
potential
involvement
transient
receptor
(TRP)
channels
NDs,
where
disrupted
homeostasis
leads
death.
capability
TRP
restore
excite
through
regulation
depending
on
level
plasma
membrane
ATPase
(PMCA)
activity
discussed
detail.
As
PMCA
simultaneously
affects
as
well
,
thus
play
vital
roles
modulating
various
types
specific
brain
are
expressed.
For
this
reason,
dysfunction
and/or
under
disrupts
neuronal
due
abnormal
levels
brain,
resulting
NDs.
This
addresses
function
controlling
pH,
which
provide
novel
targets
treating
