Brain‐X,
Journal Year:
2024,
Volume and Issue:
2(3)
Published: Sept. 1, 2024
Abstract
Hearing
sound
and
responding
to
external
internal
mechanical
stimuli
requires
specific
proteins
as
mechanotransducers
that
convert
forces
into
biological
signals.
However,
our
understanding
of
the
mechanotransduction
process
in
inner
ear
is
still
incomplete.
Mechanically
activated
ion
channels,
PIEZO1
PIEZO2,
are
widely
distributed
throughout
body
play
essential
roles.
Recent
studies
have
discovered
Piezo
channels
expressed
hair
cells,
suggesting
their
potential
involvement
auditory
perception.
This
review
summarizes
existing
discoveries
about
including
structure,
mechanogating
mechanisms,
general
physiological
roles,
explicitly
focusing
on
systems.
roles
ultrasound
perception,
generation
anomalous
current,
cell
development,
potentially
normal
mechanoelectrical
transduction
cells.
Collectively,
this
aims
provide
a
new
perspective
channel
its
Neuroglia,
Journal Year:
2024,
Volume and Issue:
5(4), P. 410 - 444
Published: Oct. 21, 2024
Microglia,
the
unique
and
motile
immune
cells
of
central
nervous
system
(CNS),
function
as
a
security
guard
in
maintaining
CNS
homeostasis,
primarily
through
calcium
signaling.
The
dynamics
microglia
control
important
functions
such
phagocytosis,
cytokine
release,
migration.
Calcium
dysregulation
has
been
linked
to
several
disorders,
like
Alzheimer’s
disease
(AD),
Parkinson’s
(PD),
multiple
sclerosis
(MS),
ischemic
stroke
(IS).
entering
channels
voltage-gated
(VGCCs),
store-operated
entry
(SOCE),
transient
receptor
potential
(TRP)
is
essential
for
microglial
activation
pro-inflammatory
responses.
Under
pathological
conditions,
formation
amyloid-β
plaques
AD,
aggregation
α-synuclein
PD,
oxidative
stress
MS,
exacerbates
neuroinflammation,
mitochondrial
dysfunction,
neurodegeneration.
Therapeutic
strategies
targeting
signaling
pathways,
using
channel
blockers
antioxidant
interventions,
show
promise
alleviating
slowing
down
progression.
This
review
summarizes
underlying
mechanisms
therapeutic
benefits
restoring
balance
disorders.
Acta Physiologica,
Journal Year:
2025,
Volume and Issue:
241(2)
Published: Jan. 13, 2025
Octopamine
in
the
Drosophila
brain
has
a
neuromodulatory
role
similar
to
that
of
noradrenaline
mammals.
After
release
from
Tdc2
neurons,
octopamine/tyramine
may
trigger
intracellular
Ca
We
expressed
Octopamine-stimulated
In
optic
lobes,
astrocytes,
not
appear
be
sole
responders
low
concentration
octopamine
signals,
and
therefore
likely
drive
synaptic
plasticity
visual
processing.
Given
interconnectivity
lobes
with
other
regions,
octopaminergic
signals
acting
through
lobe
astrocytes
also
influence
higher-order
functions
including
learning
memory.
Biomolecules,
Journal Year:
2024,
Volume and Issue:
14(7), P. 833 - 833
Published: July 11, 2024
Microglia,
as
resident
macrophages
in
the
central
nervous
system,
play
a
multifunctional
role
pathogenesis
of
Alzheimer’s
disease
(AD).
Their
clustering
around
amyloid-β
(Aβ)
deposits
is
core
pathological
feature
AD.
Recent
advances
single-cell
RNA
sequencing
(scRNA-seq)
and
single-nucleus
(snRNA-seq)
have
revealed
dynamic
changes
microglial
phenotypes
over
time
across
different
brain
regions
during
aging
AD
progression.
As
advances,
microglia
primarily
exhibit
impaired
phagocytosis
Aβ
tau,
along
with
release
pro-inflammatory
cytokines
that
damage
synapses
neurons.
Targeting
has
emerged
potential
therapeutic
approach
for
Treatment
strategies
involving
can
be
broadly
categorized
into
two
aspects:
(1)
enhancing
function:
This
involves
augmenting
their
phagocytic
ability
against
cellular
debris
(2)
mitigating
neuroinflammation:
Strategies
include
inhibiting
TNF-α
signaling
to
reduce
neuroinflammatory
response
triggered
by
microglia.
Clinical
trials
exploring
microglia-related
approaches
treatment
garnered
attention.
Additionally,
natural
products
show
promise
beneficial
effects
suppressing
inflammatory
responses.
Clarifying
dynamics,
understanding
roles,
novel
will
advance
our
fight
PLoS ONE,
Journal Year:
2025,
Volume and Issue:
20(1), P. e0317683 - e0317683
Published: Jan. 22, 2025
Motor
dysfunction
and
muscle
atrophy
are
typical
symptoms
of
patients
with
spinal
cord
injury
(SCI).
Exercise
training
is
a
conventional
physical
therapy
after
SCI,
but
exercise
intervention
alone
may
have
limited
efficacy
in
reducing
secondary
promoting
nerve
regeneration
functional
remodeling.
Our
previous
research
found
that
intramedullary
pressure
SCI
one
the
key
factors
affecting
prognosis.
It
has
been
reported
GsMTx-4,
specific
blocker
mechanosensitive
ion
channels
Piezo1,
can
protect
integrity
neuromuscular
junction
promote
regeneration,
thus
potential
as
therapeutic
agent
for
SCI.
In
this
study,
we
observed
combined
separate
effect
GsMTx-4
on
structure
soleus
motor
function
rats
At
42
days
post-injury,
compared
rats,
Basso–Beattie–Bresnahan
score
(P
=
0.0007)
Gait
Symmetry
0.0002)
were
significantly
improved
combination
therapy.
On
histology
rat
muscle,
treatment
increased
wet
weight
ratio,
fiber
cross-sectional
area
acetylcholinesterase
(all
P<0.0001).
tissue,
neuron
counts
BDNF
levels,
reduced
percentage
TUNEL-positive
cells
physiology
succinate
dehydrogenase
expression
(P<0.0001),
while
α-glycerophosphate
(P<0.0001)
GDF8
protein
0.0008)
decreased.
Results
indicate
effectively
improves
histopathology
enhancing
function.
This
study
was
conducted
animal
models,
it
offers
insights
treatment,
advancing
understanding
lower
limb
pathology
post-SCI.
Further
needed
clinical
validation
future.
Channels,
Journal Year:
2025,
Volume and Issue:
19(1)
Published: April 13, 2025
Microglia,
the
central
nervous
system
(CNS)
resident
immune
cells,
are
pivotal
in
regulating
neurodevelopment,
maintaining
neural
homeostasis,
and
mediating
neuroinflammatory
responses.
Recent
research
has
highlighted
importance
of
mechanotransduction,
process
by
which
cells
convert
mechanical
stimuli
into
biochemical
signals,
microglial
activity.
Among
various
mechanosensitive
channels,
Piezo1
emerged
as
a
key
player
microglia,
influencing
their
behavior
under
both
physiological
pathological
conditions.
This
review
focuses
on
expression
role
particularly
context
neuroinflammation
tumorigenesis.
We
explore
how
mediates
responses
to
changes
within
CNS,
such
alterations
tissue
stiffness
fluid
shear
stress,
common
conditions
like
multiple
sclerosis,
Alzheimer's
disease,
cerebral
ischemia,
gliomas.
The
also
discusses
potential
targeting
for
therapeutic
intervention,
given
its
involvement
modulation
activity
impact
disease
progression.
integrates
findings
from
recent
studies
provide
comprehensive
overview
Piezo1's
mechanistic
pathways
function.
These
insights
illuminate
new
possibilities
developing
targeted
therapies
addressing
CNS
disorders
with
mechanics.
International Journal of Neuroscience,
Journal Year:
2025,
Volume and Issue:
unknown, P. 1 - 23
Published: April 25, 2025
Piezo1
is
a
ubiquitously
expressed
non-selective
cation
channel
protein
found
across
various
species.
It
possesses
the
ability
to
detect
and
respond
external
mechanical
forces,
converting
cues
into
intracellular
bioelectrical
events,
thereby
facilitating
propagation
of
electrochemical
signals.
Within
nervous
system,
integral
synaptogenesis
myelination,
modulation
pro-inflammatory
mediators,
neuropathic
pain,
cognitive
processes,
angiogenesis,
regulation
cerebral
hemodynamics,
consequently
impacting
pathogenesis
progression
neurological
disorders.
This
review
meticulously
summarizes
synthesizes
existing
literature
provide
an
exhaustive
overview
Piezo1's
roles
mechanisms
in
spectrum
diseases,
including
neurodegenerative
disorders,
cerebrovascular
accidents,
traumatic
brain
injuries,
gliomas,
multiple
sclerosis,
epilepsy.
Additionally,
it
explores
potential
therapeutic
applications
targeting
Piezo1.
The
discussion
also
encompasses
current
research
limitations,
imperative
need
for
future
investigations,
prospective
strategies.
Our
analysis
indicates
that
susceptibility
gene
conditions,
its
expression
inhibition
may
confer
benefits.
In
summary,
this
comprehensive
offers
novel
insights
involvement
diseases
establishes
theoretical
groundwork
development
Piezo1-targeted
interventions.