Redox Biology,
Год журнала:
2023,
Номер
67, С. 102926 - 102926
Опубликована: Окт. 16, 2023
Mitochondria
are
a
main
source
of
cellular
energy.
Oxidative
phosphorylation
(OXPHOS)
is
the
major
process
aerobic
respiration.
Enzyme
complexes
electron
transport
chain
(ETC)
pump
protons
to
generate
protonmotive
force
(Δp)
that
drives
OXPHOS.
Complex
I
an
entry
point
into
ETC.
oxidizes
nicotinamide
adenine
dinucleotide
(NADH)
and
transfers
electrons
ubiquinone
in
reaction
coupled
with
proton
pumping.
also
produces
reactive
oxygen
species
(ROS)
under
various
conditions.
The
enzymatic
activities
complex
can
be
regulated
by
metabolic
conditions
serves
as
regulatory
node
ROS
plays
diverse
roles
cell
metabolism
ranging
from
physiologic
pathologic
Progress
our
understanding
indicates
release
important
signaling
functions.
Increasing
evidence
suggests
mismatch
energy
production
demand.
In
this
article,
we
review
role
sensing
acute
hypoxia.
Circulation Research,
Год журнала:
2024,
Номер
135(2), С. 372 - 396
Опубликована: Июль 4, 2024
Despite
clinical
and
scientific
advancements,
heart
failure
is
the
major
cause
of
morbidity
mortality
worldwide.
Both
mitochondrial
dysfunction
inflammation
contribute
to
development
progression
failure.
Although
crucial
reparative
healing
following
acute
cardiomyocyte
injury,
chronic
damages
heart,
impairs
function,
decreases
cardiac
output.
Mitochondria,
which
comprise
one
third
volume,
may
prove
a
potential
therapeutic
target
for
Known
primarily
energy
production,
mitochondria
are
also
involved
in
other
processes
including
calcium
homeostasis
regulation
cellular
apoptosis.
Mitochondrial
function
closely
related
morphology,
alters
through
dynamics,
thus
ensuring
that
needs
cell
met.
However,
failure,
changes
substrate
use
lead
impaired
myocyte
function.
This
review
discusses
cristae
role
contact
site
organizing
system
complex
ultrastructure
changes.
Additionally,
this
covers
mitochondria-endoplasmic
reticulum
sites,
communication
via
nanotunnels,
altered
metabolite
production
during
We
highlight
these
often-neglected
factors
promising
targets
Advanced Materials,
Год журнала:
2024,
Номер
36(18)
Опубликована: Янв. 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.
Experimental & Molecular Medicine,
Год журнала:
2024,
Номер
56(1), С. 66 - 85
Опубликована: Янв. 4, 2024
Abstract
Mitochondria
have
been
primarily
considered
intracellular
organelles
that
are
responsible
for
generating
energy
cell
survival.
However,
accumulating
evidence
suggests
mitochondria
secreted
into
the
extracellular
space
under
physiological
and
pathological
conditions,
these
play
diverse
roles
by
regulating
metabolism,
immune
response,
or
differentiation/maturation
in
target
cells.
Furthermore,
increasing
amount
of
research
shows
therapeutic
effects
local
systemic
administration
various
disease
models.
These
findings
led
to
growing
interest
exploring
as
potential
agents.
Here,
we
discuss
emerging
extracellularly
shed
light
on
their
functions
beyond
production.
Additionally,
provide
information
outcomes
mitochondrial
transplantation
animal
models
diseases
an
update
ongoing
clinical
trials,
underscoring
using
a
novel
intervention.
Phytotherapy Research,
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 4, 2025
Resveratrol
(RES),
a
natural
polyphenolic
compound,
has
garnered
significant
attention
for
its
therapeutic
potential
in
various
pathological
conditions.
This
review
explores
how
RES
modulates
mitophagy-the
selective
autophagic
degradation
of
mitochondria
essential
maintaining
cellular
homeostasis.
promotes
the
initiation
and
execution
mitophagy
by
enhancing
PINK1/Parkin-mediated
mitochondrial
clearance,
reducing
reactive
oxygen
species
production,
mitigating
apoptosis,
thereby
preserving
integrity.
Additionally,
regulates
through
activation
key
molecular
targets
such
as
AMP-activated
protein
kinase
(AMPK),
mechanistic
target
rapamycin
(mTOR),
deacetylases
(SIRT1
SIRT3),
quality
control
(MQC)
pathways,
demonstrating
substantial
effects
multiple
disease
models.
We
provide
detailed
account
biosynthetic
pharmacokinetics,
metabolic
characteristics
RES,
focusing
on
role
modulation
implications
medical
applications.
Potential
adverse
associated
with
clinical
use
are
also
discussed.
Despite
promising
properties,
application
is
limited
issues
bioavailability
pharmacokinetic
profiles.
Future
research
should
concentrate
developing
derivatives
that
precisely
modulate
mitophagy,
unlocking
new
avenues
therapy.
Highlights•RQ
is
present
in
mitochondria
isolated
from
certain
mouse
and
human
tissues•RQ
carries
electrons
to
fumarate
as
the
electron
acceptor,
independently
of
O2
levels•The
ETC
can
be
reprogrammed
RQ/fumarate
pathway
using
genetic
pharmacologic
tools•Reprogramming
mitigates
hypoxia-induced
damage
vitro
vivoSummaryUbiquinone
(UQ),
only
known
carrier
mammalian
transport
chain
(ETC),
preferentially
delivers
terminal
acceptor
oxygen
(O2).
In
hypoxia,
ubiquinol
(UQH2)
diverts
these
onto
instead.
Here,
we
identify
rhodoquinone
(RQ),
an
detected
purified
tissues
that
through
reversal
succinate
dehydrogenase,
independent
environmental
levels.
The
strictly
vivo
undetectable
cultured
cells.
Using
tools
reprogram
UQ/O2
pathway,
establish
distinct
ETCs
support
unique
programs
mitochondrial
function
RQ
confers
protection
upon
hypoxia
exposure
vivo.
Thus,
discovering
presence
mammals,
unveil
a
tractable
therapeutic
strategy
exploits
flexibility
ameliorate
hypoxia-related
conditions.Graphical
abstract
