Cell Reports,
Год журнала:
2025,
Номер
44(1), С. 115154 - 115154
Опубликована: Янв. 1, 2025
Recent
research
has
shown
that
mtDNA-deficient
cancer
cells
(ρ0
cells)
acquire
mitochondria
from
tumor
stromal
to
restore
respiration,
facilitating
formation.
We
investigated
the
role
of
Miro1,
an
adaptor
protein
involved
in
movement
along
microtubules,
this
phenomenon.
Inducible
Miro1
knockout
(Miro1KO)
mice
markedly
delayed
formation
after
grafting
ρ0
cells.
Miro1KO
with
fluorescently
labeled
revealed
delay
was
due
hindered
mitochondrial
transfer
grafted
B16
cells,
which
impeded
recovery
respiration
and
growth.
led
perinuclear
accumulation
impaired
mobility
network.
In
vitro
experiments
decreased
association
compromising
via
tunneling
nanotubes
(TNTs)
mesenchymal
Here
we
show
horizontal
mouse
melanoma
models
vivo
its
involvement
TNTs.
Abstract
Current
research
on
human
aging
has
largely
been
guided
by
the
milestone
paper
“hallmarks
of
aging,”
which
were
first
proposed
in
seminal
2013
Lopez‐Otin
et
al.
Most
studies
have
focused
one
hallmark
at
a
time,
asking
whether
underlying
molecular
perturbations
are
sufficient
to
drive
process
and
its
associated
phenotypes.
More
recently,
researchers
begun
investigate
phenotypes
driven
concurrent
pathways
linked
not
but
multiple
hallmarks
they
present
different
patterns
organs
systems
over
time.
Indeed,
preliminary
results
suggest
that
more
complex
interactions
between
must
be
considered
addressed,
if
we
develop
interventions
successfully
promote
healthy
and/or
delay
aging‐associated
dysfunction
diseases.
Here,
summarize
some
latest
work
views
interplay
aging,
with
specific
focus
mitochondrial
dysfunction.
this
represents
significant
example
crosstalk
effects
an
intervention
targeted
may
others.
A
better
knowledge
these
interconnections,
their
cause‐effect
relationships,
spatial
temporal
sequence,
will
very
beneficial
for
whole
field
identification
effective
promoting
old
age.
AJP Cell Physiology,
Год журнала:
2023,
Номер
325(4), С. C862 - C884
Опубликована: Авг. 14, 2023
Mitochondria
control
cellular
functions
through
their
metabolic
role.
Recent
research
that
has
gained
considerable
attention
is
ability
to
transfer
between
cells.
This
the
potential
of
improving
in
pathological
or
energy-deficit
conditions,
but
little
known
about
role
mitochondrial
sustaining
homeostasis.
Few
studies
have
investigated
skeletal
muscle
as
a
source
healthy
mitochondria
can
be
transferred
other
cell
types.
Thus,
we
isolated
intermyofibrillar
from
murine
and
incubated
them
with
host
We
observed
dose-
time-dependent
increases
incorporation
into
myoblasts.
resulted
elongated
networks
an
enhancement
bioenergetic
profile
Mitochondrial
donation
also
rejuvenated
functional
capacities
myoblasts
when
respiration
efficiency
lysosomal
function
were
inhibited
by
complex
I
inhibitor
rotenone
bafilomycin
A,
respectively.
was
accomplished
via
tunneling
nanotubes,
extracellular
vesicles,
gap
junctions,
macropinocytosis
internalization.
Murine
effectively
human
fibroblast
cells
having
DNA
mutations,
resulting
augmented
dynamics
functions.
improved
diminishing
reactive
oxygen
species
(ROS)
emission
diseased
Our
findings
suggest
donor
integrated
both
functionally
compromised
leading
structural
refinement
respiratory
boost.
trafficking
reprogramming
maintain
revitalize
tissue
homeostasis
could
useful
therapeutic
strategy
treating
diseases.NEW
&
NOTEWORTHY
In
our
study,
shown
mouse
transplanted
mutations.
augmentation
International Journal of Molecular Sciences,
Год журнала:
2023,
Номер
24(21), С. 15788 - 15788
Опубликована: Окт. 31, 2023
Due
to
their
beneficial
effects
in
an
array
of
diseases,
Mesenchymal
Stromal
Cells
(MSCs)
have
been
the
focus
intense
preclinical
research
and
clinical
implementation
for
decades.
MSCs
multilineage
differentiation
capacity,
support
hematopoiesis,
secrete
pro-regenerative
factors
exert
immunoregulatory
functions
promoting
homeostasis
resolution
injury/inflammation.
The
main
include
modulation
immune
cells
(macrophages,
neutrophils,
lymphocytes),
secretion
antimicrobial
peptides,
transfer
mitochondria
(Mt)
injured
cells.
These
actions
can
be
enhanced
by
priming
(i.e.,
licensing)
prior
exposure
deleterious
microenvironments.
Preclinical
evidence
suggests
that
therapeutic
a
variety
pathological
states,
including
cardiac,
respiratory,
hepatic,
renal,
neurological
diseases.
One
key
emerging
is
improvement
mitochondrial
tissues
enhancing
quality
control
(MQC).
Recent
advances
understanding
cellular
MQC,
biogenesis,
mitophagy,
fission,
fusion,
helped
uncover
how
enhance
these
processes.
Specifically,
suggested
regulate
peroxisome
proliferator-activated
receptor-gamma
coactivator
1
alpha
(PGC1α)-dependent
Parkin-dependent
Mitofusins
(Mfn1/2)
or
Dynamin
Related
Protein-1
(Drp1)-mediated
fission/fusion.
In
addition,
previous
studies
also
verified
from
through
tunneling
nanotubes
via
microvesicular
transport.
Combined,
improve
functions,
thereby
contributing
injury
inflammation.
Thus,
uncovering
affect
MQC
opens
new
avenues
organ
injury,
transplantation
MSC-derived
might
represent
attractive
approach.
Frontiers in Physiology,
Год журнала:
2023,
Номер
14
Опубликована: Ноя. 15, 2023
Aging
of
human
skin
is
a
complex
process
leading
to
decline
in
homeostasis
and
regenerative
potential
this
tissue.
Mitochondria
are
important
cell
organelles
that
have
crucial
role
several
cellular
mechanisms
such
as
energy
production
free
radical
maintenance.
However,
mitochondrial
metabolism
well
processes
dynamics,
biogenesis,
degradation
varies
considerably
among
the
different
types
cells
populate
skin.
Disturbed
function
known
promote
aging
inflammation
skin,
impairment
physiological
onset
pathologies.
In
review,
we
discuss
essential
mitochondria
how
morphology,
physiology,
each
these
compartments
contributes
aging.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(2), С. 1175 - 1175
Опубликована: Янв. 18, 2024
Mitochondria
are
double-membrane
organelles
that
involved
in
energy
production,
apoptosis,
and
signaling
eukaryotic
cells.
Several
studies
conducted
over
the
past
decades
have
correlated
mitochondrial
dysfunction
with
various
diseases,
including
cerebral
ischemia,
myocardial
ischemia-reperfusion,
cancer.
Mitochondrial
transplantation
entails
importing
intact
mitochondria
from
healthy
tissues
into
diseased
damaged
to
rescue
injured
In
this
review,
different
techniques
their
clinical
applications
been
discussed.
addition,
challenges
future
directions
pertaining
its
potential
treatment
of
diseases
defective
summarized.
Clinical & Experimental Metastasis,
Год журнала:
2024,
Номер
41(5), С. 567 - 587
Опубликована: Март 15, 2024
Abstract
As
a
major
energy
source
for
cells,
mitochondria
are
involved
in
cell
growth
and
proliferation,
as
well
migration,
fate
decisions,
many
other
aspects
of
cellular
function.
Once
thought
to
be
irreparably
defective,
mitochondrial
function
cancer
cells
has
found
renewed
interest,
from
suggested
potential
clinical
biomarkers
mitochondria-targeting
therapies.
Here,
we
will
focus
on
the
effect
movement
breast
progression.
Mitochondria
move
both
within
cell,
such
localize
areas
high
energetic
need,
between
where
stroma
have
been
shown
donate
their
via
multiple
methods
including
tunneling
nanotubes.
The
donation
seen
increase
aggressiveness
chemoresistance
which
increased
recent
efforts
uncover
mechanisms
transfer.
metabolism
energetics
gaining
attention
targets,
better
understanding
implications
required
developing
effective,
targeted
therapeutics
patients.
Advanced Science,
Год журнала:
2025,
Номер
unknown
Опубликована: Фев. 28, 2025
Abstract
Lipid
metabolism
disorders
in
both
neurons
and
glial
cells
have
been
found
neurodegenerative
(ND)
patients
animal
models.
However,
the
pathological
connection
between
lipid
droplets
NDs
remains
poorly
understood.
The
recent
work
has
highlighted
utility
of
a
neuron‐specific
Arf1‐knockout
mouse
model
corresponding
for
elucidating
nexus
amyotrophic
lateral
sclerosis
(ALS)
multiple
(MS).
In
this
study,
it
is
that
Arf1
deficiency
first
induced
surplus
fatty
acid
synthesis
through
AKT‐mTORC1‐SREBP1‐FASN
axis,
which
further
triggered
endoplasmic
reticulum
(ER)‐mitochondrial
stress
cascade
via
calcium
flux.
organelle
caused
mitochondrial
DNA
(mtDNA)
to
be
released
into
cytoplasm.
Concurrently,
FASN‐driven
Arf1‐deficient
might
also
induce
accumulation
sphingolipids
lysosomes
dysfunction
autophagy
lysosomes,
promoted
lysosomal
mitochondria‐derived
extracellular
vesicles
(MDEVs)
release.
MDEVs
carried
mtDNA
microglia
activate
inflammatory
pathways
neurodegeneration.
studies
on
neuronal
(LDs)
microglial
LDs
suggest
unified
function
NDs:
activating
microglia.
This
finding
potentially
provides
new
therapeutic
strategies
NDs.