The roles of mitochondria in global and local intracellular calcium signalling
Nature Reviews Molecular Cell Biology,
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 27, 2025
Язык: Английский
Mitochondrial Calcium Regulation of Cardiac Metabolism in Health and Disease
Physiology,
Год журнала:
2024,
Номер
39(5), С. 247 - 268
Опубликована: Май 7, 2024
Oxidative
phosphorylation
is
regulated
by
mitochondrial
calcium
(Ca2+)
in
health
and
disease.
In
physiological
states,
Ca2+
enters
via
the
uniporter
rapidly
enhances
NADH
ATP
production.
However,
maintaining
homeostasis
critical:
insufficient
impairs
stress
adaptation,
overload
can
trigger
cell
death.
this
review,
we
delve
into
recent
insights
further
defining
relationship
between
dynamics
oxidative
phosphorylation.
Our
focus
on
how
such
regulation
affects
cardiac
function
disease,
including
heart
failure,
ischemia-reperfusion,
arrhythmias,
catecholaminergic
polymorphic
ventricular
tachycardia,
cardiomyopathies,
Barth
syndrome,
Friedreich's
ataxia.
Several
themes
emerge
from
data.
First,
critical
for
fuel
substrate
selection,
metabolite
import,
matching
of
supply
to
demand.
Second,
regulates
both
production
response
reactive
oxygen
species
(ROS),
balance
its
pro-
antioxidant
effects
key
it
contributes
pathological
states.
Third,
exerts
localized
electron
transport
chain
(ETC),
not
through
traditional
allosteric
mechanisms
but
rather
indirectly.
These
hinge
specific
transporters,
as
or
Na+/Ca2+
exchanger,
may
be
noticeable
acutely,
contributing
differently
phenotypes
depending
whether
transporters
are
acutely
chronically
modified.
Perturbations
these
novel
relationships
during
disease
states
either
serve
compensatory
exacerbate
impairments
Consequently,
targeting
holds
promise
a
therapeutic
strategy
variety
diseases
characterized
contractile
failure
arrhythmias.
Язык: Английский
MCU genetically altered mice suggest how mitochondrial Ca2+ regulates metabolism
Trends in Endocrinology and Metabolism,
Год журнала:
2024,
Номер
35(10), С. 918 - 928
Опубликована: Апрель 29, 2024
Язык: Английский
Early Synapse-Specific Alterations of Photoreceptor Mitochondria in the EAE Mouse Model of Multiple Sclerosis
Cells,
Год журнала:
2025,
Номер
14(3), С. 206 - 206
Опубликована: Янв. 30, 2025
Multiple
sclerosis
(MS)
is
an
inflammatory
autoimmune
disease
of
the
central
nervous
system
(CNS)
linked
to
many
neurological
disabilities.
The
visual
frequently
impaired
in
MS.
In
previous
studies,
we
observed
early
malfunctions
rod
photoreceptor
ribbon
synapses
EAE
mouse
model
MS
that
included
alterations
synaptic
vesicle
cycling
and
disturbances
presynaptic
Ca2+
homeostasis.
Since
these
events
are
highly
energy-demanding,
analyzed
whether
mitochondria,
which
play
a
major
role
energy
metabolism,
might
be
involved
at
stage.
Rod
terminals
contain
single
large
mitochondrion
next
ribbon.
present
study,
expression
functionally
relevant
mitochondrial
proteins
(MIC60,
ATP5B,
COX1,
PINK1,
DRP1)
by
high-resolution
qualitative
quantitative
immunofluorescence
microscopy,
immunogold
electron
microscopy
Western
blot
experiments.
We
decreased
mitochondria
photoreceptors
stage,
suggesting
dysfunctions
important
synapse
pathology.
Interestingly,
were
strongly
compromised
EAE,
whereas
extra-synaptic
inner
segments
remained
unchanged,
demonstrating
functional
heterogeneity
mitochondria.
Язык: Английский
Chimeric Cell Therapy Transfers Healthy Donor Mitochondria in Duchenne Muscular Dystrophy
Stem Cell Reviews and Reports,
Год журнала:
2024,
Номер
20(7), С. 1819 - 1829
Опубликована: Июль 17, 2024
Duchenne
muscular
dystrophy
(DMD)
is
a
severe
X-linked
disorder
characterized
by
dystrophin
gene
mutations
and
mitochondrial
dysfunction,
leading
to
progressive
muscle
weakness
premature
death
of
DMD
patients.
We
developed
human
Dystrophin
Expressing
Chimeric
(DEC)
cells,
created
the
fusion
myoblasts
from
normal
donors
patients,
as
foundation
for
DT-DEC01
therapy
DMD.
Our
preclinical
studies
on
mdx
mouse
models
revealed
enhanced
expression
functional
improvements
in
cardiac,
respiratory,
skeletal
muscles
after
systemic
intraosseous
DEC
administration.
The
current
study
explored
feasibility
transfer
within
which
crucial
developing
new
therapeutic
strategies
Following
staining
with
MitoTracker
Deep
Red
Green
dyes,
was
assessed
Flow
cytometry
(FACS)
confocal
microscopy.
PEG-mediated
healthy
(MB
Язык: Английский
Effects of aging on calcium channels in skeletal muscle
Frontiers in Molecular Biosciences,
Год журнала:
2025,
Номер
12
Опубликована: Март 19, 2025
In
skeletal
muscle,
calcium
is
not
only
essential
to
stimulate
and
sustain
their
contractions
but
also
for
muscle
embryogenesis,
regeneration,
energy
production
in
mitochondria,
fusion.
Different
ion
channels
contribute
achieving
the
various
functions
of
muscles.
Muscle
contraction
initiated
by
releasing
from
sarcoplasmic
reticulum
through
ryanodine
receptor
gated
mechanically
four
dihydropyridine
receptors
T-tubules.
The
influx
store-operated
sustains
stimulates
regeneration.
Mitochondrial
uniporter
allows
entry
into
mitochondria
oxidative
phosphorylation.
Aging
alters
expression
activity
these
different
channels,
resulting
a
reduction
force
generation
regeneration
capacity.
Regular
physical
training
bioactive
molecules
nutrients
can
prevent
effects
aging
on
channels.
This
review
focuses
current
knowledge
muscles’
Язык: Английский
Identification of VDAC1 as a mitochondria-related target of Duchenne muscular dystrophy based on bioinformatics analysis and in vitro experiments
International Immunopharmacology,
Год журнала:
2025,
Номер
158, С. 114836 - 114836
Опубликована: Май 12, 2025
Язык: Английский
Mitochondrial oxidative stress, calcium and dynamics in cardiac ischaemia‐reperfusion injury
The Journal of Physiology,
Год журнала:
2025,
Номер
unknown
Опубликована: Май 31, 2025
Abstract
Ischaemia–reperfusion
injury
(IRI)
is
a
major
cause
of
cardiomyocyte
damage
and
death
from
myocardial
infarction.
Oxidative
stress,
dysregulated
calcium
(Ca
2+
)
handling
disrupted
mitochondrial
dynamics
are
all
key
factors
in
IRI
can
play
role
cell
death.
Mitochondria
primary
source
oxidative
which
generated
by
electron
leak
the
respiratory
chain
complexes
oxidation
accumulated
succinate
upon
reperfusion.
The
permeability
transition
pore
(mPTP),
high
conductance
channel
that
forms
following
reperfusion
ischaemic
mitochondria,
has
been
implicated
reperfusion‐induced
Although
including
Ca
overload
stress
regulate
mPTP
opening
have
well
characterized,
composition
still
actively
investigated.
Clinically,
complicate
treatment
Therefore,
many
possible
therapeutics
to
reduce
damaging
effects
under
investigation.
Antioxidants,
pharmaceutical
approaches,
postconditioning
synthetic
polymers
investigated
for
use
IRI.
Still,
these
interest
shown
mixed
evidence
underlying
their
preclinical
clinical
research.
In
this
review
we
discuss
our
current
understanding
contributions
IRI,
where
further
clarification
mechanisms
needed
identify
potential
therapeutic
targets.
image
Язык: Английский