Advanced Materials,
Journal Year:
2024,
Volume and Issue:
36(18)
Published: Jan. 15, 2024
Abstract
Mitochondria,
widely
known
as
the
energy
factories
of
eukaryotic
cells,
have
a
myriad
vital
functions
across
diverse
cellular
processes.
Dysfunctions
within
mitochondria
serve
catalysts
for
various
diseases,
prompting
widespread
demise.
Mounting
research
on
remedying
damaged
indicates
that
constitute
valuable
target
therapeutic
intervention
against
diseases.
But
less
clinical
practice
and
lower
recovery
rate
imply
limitation
traditional
drugs,
which
need
further
breakthrough.
Nanotechnology
has
approached
favorable
regiospecific
biodistribution
high
efficacy
by
capitalizing
excellent
nanomaterials
targeting
drug
delivery.
Mitochondria‐remedying
nanodrugs
achieved
ideal
effects.
This
review
elucidates
significance
in
cells
organs,
while
also
compiling
mortality
data
related
Correspondingly,
nanodrug‐mediate
strategies
applicable
mitochondria‐remedying
disease
are
detailed,
with
full
understanding
roles
dysfunction
advantages
nanodrugs.
In
addition,
future
challenges
directions
discussed.
conclusion,
this
provides
comprehensive
insights
into
design
development
nanodrugs,
aiming
to
help
scientists
who
desire
extend
their
fields
engage
interdisciplinary
subject.
The Journal of Physiology,
Journal Year:
2024,
Volume and Issue:
unknown
Published: March 23, 2024
Abstract
Lymphatic
collecting
vessels
exhibit
spontaneous
phasic
contractions
that
are
critical
for
lymph
propulsion
and
tissue
fluid
homeostasis.
This
rhythmic
activity
is
driven
by
action
potentials
conducted
across
the
lymphatic
muscle
cell
(LMC)
layer
to
produce
entrained
contractions.
The
contraction
frequency
of
a
vessel
displays
exquisite
mechanosensitivity,
with
dynamic
range
from
<1
>20
per
minute.
A
myogenic
pacemaker
mechanism
intrinsic
LMCs
was
initially
postulated
account
pressure‐dependent
chronotropy.
Further
interrogation
into
cellular
constituents
wall
identified
non‐muscle
populations
shared
some
characteristics
interstitial
cells
Cajal,
which
have
functions
in
gastrointestinal
lower
urinary
tracts,
thus
raising
possibility
pacemaker.
However,
recent
genetic
knockout
studies
mice
support
origin
activity.
stochastic,
but
pressure‐sensitive,
sarcoplasmic
reticulum
calcium
release
(puffs
waves)
IP
3
R1
receptors,
couple
calcium‐activated
chloride
channel
Anoctamin
1,
causing
depolarisation.
resulting
electrical
integrates
highly
coupled
syncytia
through
connexin
45
modulate
diastolic
multiple
other
cation
channels
may
also
contribute
ionic
pacemaking
cycle.
Upon
reaching
threshold,
voltage‐gated
channel‐dependent
potential
fires,
nearly
synchronous
global
flash
within
LMC
drive
an
contraction.
review
summarizes
key
ion
potentially
responsible
chronotropy
various
mechanisms
regulation
could
tuning.
image
Channels,
Journal Year:
2024,
Volume and Issue:
18(1)
Published: April 11, 2024
Voltage-gated
calcium
channels
(VGCCs)
are
the
major
conduits
for
ions
(Ca2+)
within
excitable
cells.
Recent
studies
have
highlighted
non-ionotropic
functionality
of
VGCCs,
revealing
their
capacity
to
activate
intracellular
pathways
independently
ion
flow.
This
signaling
mode
plays
a
pivotal
role
in
excitation-coupling
processes,
including
gene
transcription
through
excitation-transcription
(ET),
synaptic
transmission
via
excitation-secretion
(ES),
and
cardiac
contraction
excitation-contraction
(EC).
However,
it
is
noteworthy
that
these
processes
require
extracellular
Ca2+
occupancy
channel
pore.
Analogous
"non-canonical"
characterization
exhibited
by
N-methyl-D-aspartate
receptor
(NMDA),
which
requires
without
influx
ions,
VGCC
activation
depolarization-triggered
conformational
change(s)
concomitant
with
binding
open
channel.
Here,
we
discuss
contributions
VGCCs
ES,
ET,
EC
coupling
as
macromolecules
transduces
external
stimuli
input
prior
elevating
Ca2+.
We
emphasize
recognition
ion-pore
its
contribution
excitation
precede
calcium.
The
triggered
upstroke
an
action
potential,
provides
conceptual
framework
elucidate
mechanistic
aspects
underlying
microseconds
nature
transmission,
contractility,
rapid
induction
first-wave
genes.
Nature Communications,
Journal Year:
2023,
Volume and Issue:
14(1)
Published: July 28, 2023
Abstract
Lysosomes
communicate
through
cholesterol
transfer
at
endoplasmic
reticulum
(ER)
contact
sites.
At
these
sites,
the
Niemann
Pick
C1
transporter
(NPC1)
facilitates
removal
of
from
lysosomes,
which
is
then
transferred
to
ER
for
distribution
other
cell
membranes.
Mutations
in
NPC1
result
buildup
within
leading
Niemann-Pick
Type
C
(NPC)
disease,
a
progressive
and
fatal
neurodegenerative
disorder.
The
molecular
mechanisms
connecting
loss
NPC-associated
neuropathology
remain
unknown.
Here
we
show
both
vitro
an
animal
model
NPC
disease
that
function
alters
activity
voltage-gated
calcium
channels
(Ca
V
).
Underlying
alterations
channel
localization
are
K
2.1
whose
interactions
drive
clustering
enhance
entry
fuel
neurotoxic
elevations
mitochondrial
calcium.
Targeted
disruption
2–Ca
rescues
aberrant
Ca
1.2
clustering,
elevated
calcium,
neurotoxicity
vitro.
Our
findings
provide
evidence
nanostructural
ion
characterized
by
altered
membrane
contacts,
contribute
neurodegeneration.
Journal of Pharmacological Sciences,
Journal Year:
2025,
Volume and Issue:
158(1), P. 59 - 67
Published: March 15, 2025
Vascular
smooth
muscle
cells
(VSMCs)
modulate
blood
pressure
by
adjusting
vascular
contractility.
Specific
families
of
ion
channels
that
are
expressed
in
VSMCs
regulate
membrane
potential
and
intracellular
Ca2+
concentration
([Ca2+]cyt).
Subsets
them
known
to
form
molecular
complexes
with
Ca2+-sensitive
molecules
via
scaffolding
proteins
such
as
caveolin
junctophilin.
This
enables
localized
complex-specific
signal
transduction
region
is
referred
a
microdomain.
When
hypertensive
stimuli
applied
vessels,
gene
expression
scaffold
changes
dramatically,
often
leading
depolarization
increased
[Ca2+]cyt.
As
result,
vessels
undergo
functional
remodeling
characterized
enhanced
In
addition,
the
transcription
inflammatory
genes
also
upregulated.
induces
leukocyte
infiltration
into
wall
structural
mediated
VSMC
proliferation
extracellular
matrix
remodeling.
perpetuates
state,
progressive
damage
systemic
organs.
review
summarizes
recent
findings
on
mechanisms
which
microdomains
due
their
contributions
both
summarized.
Toxics,
Journal Year:
2025,
Volume and Issue:
13(5), P. 347 - 347
Published: April 27, 2025
Octahydro-1,3,5,7-tetranitro-1,3,5,7-tetrazocine
(HMX)
is
a
globally
recognized
energetic
material
that
widely
used
in
industrial,
mining,
and
military
fields.
Like
hexahydro-1,3,5-trinitro-1,3,5-triazine
(RDX)
other
nitramine
compounds,
HMX
has
also
been
reported
to
exhibit
neurotoxicity.
However,
the
molecular
mechanisms
underlying
toxic
effects
of
remain
poorly
understood.
Therefore,
this
study
aims
investigate
neurotoxicity
induced
by
adopting
PC12
cells.
The
results
show
treatment
decreased
cell
viability
upregulated
intracellular
free
calcium
ions
(Ca2+)
Furthermore,
caused
aggravated
oxidative
stress
cells,
as
evidenced
upregulations
reactive
oxygen
species
(ROS)
malondialdehyde
(MDA).
Intracellular
biochemical
assays
demonstrated
loss
mitochondrial
membrane
potential
Notably,
altered
expression
brain-derived
neurotrophic
factor
(BDNF)
ionotropic
glutamate
receptors
(iGluRs),
well
an
abnormal
transcription
profile,
were
observed
cells
treated
HMX.
These
findings
suggest
exerts
on
involved
stress,
disturbances
Ca2+
BDNF,
accompanied
aberrant
iGluRs.
Overall,
present
helps
us
better
understand
health
hazards
associated
with
provides
valuable
insights
for
developing
protection
standards
related
exposure.
Biochemical Society Transactions,
Journal Year:
2024,
Volume and Issue:
52(4), P. 1617 - 1629
Published: June 27, 2024
Neurons
are
highly
specialised
cells
that
need
to
relay
information
over
long
distances
and
integrate
signals
from
thousands
of
synaptic
inputs.
The
complexity
neuronal
function
is
evident
in
the
morphology
their
plasma
membrane
(PM),
by
far
most
intricate
all
cell
types.
Yet,
within
neuron
lies
an
organelle
whose
architecture
adds
another
level
this
morphological
sophistication
-
endoplasmic
reticulum
(ER).
Neuronal
ER
abundant
body
extends
distant
axonal
terminals
postsynaptic
dendritic
spines.
It
also
adopts
structures
like
spine
apparatus
postsynapse
cisternal
axon
initial
segment.
At
contact
sites
(MCSs)
between
PM,
two
membranes
come
close
proximity
create
hubs
lipid
exchange
Ca2+
signalling
called
ER-PM
junctions.
development
electron
light
microscopy
techniques
extended
our
knowledge
on
physiological
relevance
MCSs.
Equally
important
was
identification
PM
partners
interact
these
junctions,
notably
STIM-ORAI
VAP-Kv2.1
pairs.
functions
junctions
neurons
being
increasingly
explored,
but
molecular
composition
role
dynamics
less
clear.
This
review
aims
outline
current
state
research
topic
contacts.
Specifically,
we
will
summarise
involvement
different
classes
channels
discuss
neuropathology
propose
directions
for
further
research.
