Abstract
Mitochondria
are
versatile
and
complex
organelles
that
can
continuously
communicate
interact
with
the
cellular
milieu.
Deregulated
communication
between
mitochondria
host
cells/organelles
has
significant
consequences
is
an
underlying
factor
of
many
pathophysiological
conditions,
including
process
aging.
During
aging,
lose
function,
mitocellular
pathways
break
down;
mitochondrial
dysfunction
interacts
dyscommunication,
forming
a
vicious
circle.
Therefore,
strategies
to
protect
function
promote
effective
increase
healthy
lifespan
longevity,
which
might
be
new
treatment
paradigm
for
age-related
disorders.
In
this
review,
we
comprehensively
discuss
signal
transduction
mechanisms
inter-
intracellular
communication,
as
well
interactions
hallmarks
This
review
emphasizes
indispensable
position
in
aging
organisms,
crucial
signaling
hubs.
addition,
also
specifically
focus
on
status
mitochondria-targeted
interventions
provide
potential
therapeutic
targets
diseases.
Graphical
Mitochondrion,
Journal Year:
2025,
Volume and Issue:
82, P. 102022 - 102022
Published: Feb. 27, 2025
Mitochondria,
essential
for
cellular
energy,
are
crucial
in
neurodegenerative
disorders
(NDDs)
and
their
age-related
progression.
This
review
highlights
mitochondrial
dynamics,
mitovesicles,
homeostasis,
organelle
communication.
We
examine
impacts
from
aging
NDDs,
focusing
on
protein
aggregation
dysfunction.
Prospective
therapeutic
approaches
include
enhancing
mitophagy,
improving
respiratory
chain
function,
maintaining
calcium
lipid
balance,
using
microRNAs,
transfer
to
protect
function.
These
strategies
underscore
the
role
of
health
neuronal
survival
cognitive
functions,
offering
new
opportunities.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(2), P. 1175 - 1175
Published: Jan. 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.
ACS Nano,
Journal Year:
2024,
Volume and Issue:
18(37), P. 25372 - 25404
Published: Sept. 3, 2024
Mitochondria,
pivotal
organelles
governing
cellular
biosynthesis,
energy
metabolism,
and
signal
transduction,
maintain
dynamic
equilibrium
through
processes
such
as
biogenesis,
fusion,
fission,
mitophagy.
Growing
evidence
implicates
mitochondrial
dysfunction
in
a
spectrum
of
respiratory
diseases
including
acute
lung
injury/acute
distress
syndrome,
bronchial
asthma,
pulmonary
fibrosis,
chronic
obstructive
disease,
cancer.
Consequently,
identifying
methods
capable
ameliorating
damaged
function
is
crucial
for
the
treatment
diseases.
Extracellular
vesicles
(EVs),
nanosized
membrane
released
by
cells
into
extracellular
space,
facilitate
intercellular
communication
transferring
bioactive
substances
or
signals
between
organs.
Recent
studies
have
identified
abundant
components
within
specific
subsets
EVs,
termed
(mitoEVs),
whose
contents
compositions
vary
with
disease
progression.
Moreover,
mitoEVs
demonstrated
reparative
functions
injured
recipient
cells.
However,
comprehensive
understanding
currently
lacking,
limiting
their
clinical
translation
prospects.
This
Review
explores
classification,
functional
cargo,
biological
effects
mitoEVs,
focus
on
role
Emphasis
placed
potential
markers
innovative
therapeutic
strategies
diseases,
offering
fresh
insights
mechanistic
drug
development
various
disorders.
Frontiers in Endocrinology,
Journal Year:
2024,
Volume and Issue:
14
Published: Jan. 8, 2024
Recent
evidence
from
our
lab
and
others
suggests
that
metabolic
reprogramming
of
immune
cells
drives
changes
in
cell
phenotypes
along
the
inflammatory-to-reparative
spectrum
plays
a
critical
role
mediating
inflammatory
responses
to
cardiac
injury
(e.g.
hypertension,
myocardial
infarction).
However,
factors
drive
are
not
fully
understood.
Extracellular
vesicles
(EVs)
recognized
for
their
ability
transfer
cargo
such
as
microRNAs
remote
sites
influence
remodeling.
Furthermore,
conditions
obesity
syndrome,
which
implicated
majority
cardiovascular
disease
(CVD)
cases,
can
skew
production
EVs
toward
pro-inflammatory
phenotypes.
In
this
mini-review,
we
discuss
mechanisms
by
may
metabolism
during
associated
with
syndrome
disrupt
normal
EV
function.
We
also
potential
sources
cardio-protective
anti-inflammatory
EVs,
brown
adipose
tissue.
Finally,
implications
future
therapeutics.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: April 3, 2024
To
identify
age-related
plasma
extracellular
vehicle
(EVs)
phenotypes
in
healthy
adults.
EV
proteomics
by
high-resolution
mass
spectrometry
to
evaluate
protein
stability
and
discover
age-associated
proteins
(n=4
with
4
serial
freeze-thaws
each);
validation
flow
cytometry
cytokine
quantification
multiplex
ELISA
(n=28
donors,
aged
18-83
years);
of
WI-38
fibroblast
cell
proliferation
response
co-culture
PKH67-labeled
young
old
EVs.
The
samples
from
these
specimens
were
previously
characterized
for
bilayer
structure,
intra-vesicle
mitochondria
cytokines,
hematopoietic
cell-related
surface
markers.
Compared
matched
exo-EVs
(EV-depleted
supernatants),
endo-EVs
(EV-associated)
had
higher
mean
TNF-α
IL-27,
lower
IL-6,
IL-11,
IFN-γ,
IL-17A/F,
similar
IL-1β,
IL-21,
IL-22
concentrations.
Some
endo-EV
exo-EV
concentrations
correlated,
including
TNF-α,
but
not
IL-21
or
IL-22.
Endo-EV
IFN-γ
IL-17A/F
declined
age.
By
confirmed
cytometry,
we
identified
decline
fibrinogen
(FGA,
FGB
FGG)
Age-related
indicated
predominant
origins
the
liver
innate
immune
system.
cells
(>95%)
internalized
amounts
EVs,
that
PKH67-EVs,
particularly
underwent
significantly
greater
proliferation.
cytokines
function
as
different
biomarkers.
observed
aging
phenotype
reflected
a
downregulation
subpopulations
consistent
absence
pro-coagulant
pro-inflammatory
condition
common
disease.
Autophagy,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Oct. 26, 2024
Cancer
cells
compensate
with
increasing
mitochondria-derived
vesicles
(MDVs)
to
maintain
mitochondrial
homeostasis,
when
canonical
MAP1LC3B/LC3B
(microtubule
associated
protein
1
light
chain
3
beta)-mediated
mitophagy
is
lacking.
MDVs
promote
the
transport
of
components
into
extracellular
(EVs)
and
induce
tumor
metastasis.
Although
HSP90
(heat
shock
90)
chaperones
hundreds
client
proteins
its
inhibitors
suppress
tumors,
inhibitors-related
chemotherapy
unexpected
Herein,
we
find
that
inhibitor
causes
damage
but
stimulates
low
LC3-induced
release
MDVs-derived
EVs.
However,
why
LC3
decreases
what
transcriptional
regulatory
mechanism
formation
under
inhibition
remain
unknown.
Because
TFEB
(transcription
factor
EB)
most
important
transcription
factor,
HCFC1
(host
cell
C1)
regulates