Frontiers in Physiology,
Journal Year:
2024,
Volume and Issue:
15
Published: Jan. 29, 2024
Mitochondria
are
energy
factories
that
sustain
life
activities
in
the
body,
and
their
dysfunction
can
cause
various
metabolic
diseases
threaten
human
health.
Mitophagy,
an
essential
intracellular
mitochondrial
quality
control
mechanism,
maintain
cellular
homeostasis
by
removing
damaged
mitochondria
participating
developing
diseases.
Research
has
confirmed
exercise
regulate
mitophagy
levels,
thereby
exerting
protective
effects
This
article
reviews
role
of
diseases,
on
mitophagy,
potential
mechanisms
exercise-regulated
intervention
providing
new
insights
for
future
basic
clinical
research
interventions
to
prevent
treat
Molecular Cancer,
Journal Year:
2024,
Volume and Issue:
23(1)
Published: Jan. 24, 2024
Abstract
Eukaryotic
cells
engage
in
autophagy,
an
internal
process
of
self-degradation
through
lysosomes.
Autophagy
can
be
classified
as
selective
or
non-selective
depending
on
the
way
it
chooses
to
degrade
substrates.
During
damaged
and/or
redundant
organelles
like
mitochondria,
peroxisomes,
ribosomes,
endoplasmic
reticulum
(ER),
lysosomes,
nuclei,
proteasomes,
and
lipid
droplets
are
selectively
recycled.
Specific
cargo
is
delivered
autophagosomes
by
specific
receptors,
isolated
engulfed.
Selective
autophagy
dysfunction
closely
linked
with
cancers,
neurodegenerative
diseases,
metabolic
disorders,
heart
failure,
etc.
Through
reviewing
latest
research,
this
review
summarized
molecular
markers
important
signaling
pathways
for
its
significant
role
cancers.
Moreover,
we
conducted
a
comprehensive
analysis
small-molecule
compounds
targeting
their
potential
application
anti-tumor
therapy,
elucidating
underlying
mechanisms
involved.
This
aims
supply
scientific
references
development
directions
biological
drug
discovery
future.
Advanced Science,
Journal Year:
2024,
Volume and Issue:
11(17)
Published: Feb. 21, 2024
The
regeneration
of
bone
defects
in
diabetic
patients
still
faces
challenges,
as
the
intrinsic
healing
process
is
impaired
by
hyperglycemia.
Inspired
discovery
that
endoplasmic
reticulum
(ER)
a
state
excessive
stress
and
dysfunction
under
hyperglycemia,
leading
to
osteogenic
disorder,
novel
engineered
exosome
proposed
modulate
ER
homeostasis
for
restoring
function
mesenchymal
stem
cells
(MSCs).
results
indicate
constructed
exosomes
efficiently
regulate
dramatically
facilitate
MSCs
hyperglycemic
niche.
Additionally,
underlying
therapeutic
mechanism
elucidated.
reveal
can
directly
provide
recipient
with
SHP2
activation
mitophagy
elimination
mtROS,
which
immediate
cause
dysfunction.
To
maximize
effect
exosomes,
high-performance
hydrogel
self-healing,
bioadhesive,
exosome-conjugating
properties
applied
encapsulate
vivo
application.
In
vivo,
evaluation
defect
repair
models
demonstrates
delivering
system
intensively
enhance
osteogenesis.
These
findings
crucial
insight
into
design
biological
homeostasis-based
tissue-engineering
strategies
regeneration.
Phytotherapy Research,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 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.
International Journal of Molecular Sciences,
Journal Year:
2025,
Volume and Issue:
26(1), P. 380 - 380
Published: Jan. 4, 2025
Plant
secondary
metabolites
(PSMs)
are
a
diverse
group
of
bioactive
compounds,
including
flavonoids,
polyphenols,
saponins,
and
terpenoids,
which
have
been
recognised
for
their
critical
role
in
modulating
cellular
functions.
This
review
provides
comprehensive
analysis
the
effects
PSMs
on
mitochondrial
health,
with
particular
emphasis
therapeutic
potential.
Emerging
evidence
shows
that
these
improve
function
by
reducing
oxidative
stress,
promoting
biogenesis,
regulating
key
processes
such
as
apoptosis
mitophagy.
Mitochondrial
dysfunction,
hallmark
many
pathologies,
neurodegenerative
disorders,
cardiovascular
diseases,
metabolic
syndrome,
has
shown
to
benefit
from
protective
PSMs.
Recent
studies
show
can
dynamics,
stabilise
membranes,
enhance
bioenergetics,
offering
significant
promise
prevention
treatment
mitochondrial-related
diseases.
The
molecular
mechanisms
underlying
effects,
modulation
signalling
pathways
direct
interactions
proteins,
discussed.
integration
into
strategies
is
highlighted
promising
avenue
improving
efficacy
while
minimising
side
commonly
associated
synthetic
drugs.
also
highlights
need
future
research
elucidate
specific
roles
individual
synergistic
within
complex
plant
matrices,
may
further
optimise
utility.
Overall,
this
work
valuable
insights
health
potential
natural
agents
targeting
dysfunction.
Signal Transduction and Targeted Therapy,
Journal Year:
2025,
Volume and Issue:
10(1)
Published: Jan. 9, 2025
Abstract
Mitochondria
are
essential
for
cellular
function
and
viability,
serving
as
central
hubs
of
metabolism
signaling.
They
possess
various
metabolic
quality
control
mechanisms
crucial
maintaining
normal
activities.
Mitochondrial
genetic
disorders
can
arise
from
a
wide
range
mutations
in
either
mitochondrial
or
nuclear
DNA,
which
encode
proteins
other
contents.
These
defects
lead
to
breakdown
metabolism,
such
the
collapse
oxidative
phosphorylation,
one
mitochondria’s
most
critical
functions.
diseases,
common
group
disorders,
characterized
by
significant
phenotypic
heterogeneity.
Clinical
symptoms
manifest
systems
organs
throughout
body,
with
differing
degrees
forms
severity.
The
complexity
relationship
between
mitochondria
diseases
results
an
inadequate
understanding
genotype-phenotype
correlation
these
historically
making
diagnosis
treatment
challenging
often
leading
unsatisfactory
clinical
outcomes.
However,
recent
advancements
research
technology
have
significantly
improved
our
management
conditions.
translations
mitochondria-related
therapies
actively
progressing.
This
review
focuses
on
physiological
mitochondria,
pathogenesis
potential
diagnostic
therapeutic
applications.
Additionally,
this
discusses
future
perspectives
diseases.
Cell Communication and Signaling,
Journal Year:
2025,
Volume and Issue:
23(1)
Published: Jan. 28, 2025
Oxidative
stress-associated
proximal
tubular
cells
(PTCs)
damage
is
an
important
pathogenesis
of
hypertensive
renal
injury.
We
previously
reported
the
protective
effect
VEGFR3
in
salt-sensitive
hypertension.
However,
specific
mechanism
underlying
role
kidney
during
overactivation
renin-angiotensin-aldosterone
system
remains
unclear.
In
present
study,
nephropathy
was
established
by
angiotensin
II
(Ang
II).
found
that
highly
increased
PTCs
Ang
II-infused
mice.
Activation
mitigated
dysfunction,
pathological
damage,
and
oxidative
stress
II-induced
Moreover,
we
restored
mitophagy
deficiency
induced
both
vivo
vitro
to
alleviate
injury
PTCs.
Furthermore,
experiment
demonstrated
improved
abnormal
enhancing
PARKIN
mitochondrial
translocation.
LC-MS/MS
Co-IP
assays
identified
HSPA1L
as
interacted
protein
VEGFR3,
which
promoted
translocation
PARKIN.
Mechanistically,
disorder
domain
bound
HSPA1L,
crotonylation
modification
at
K130
required
for
regulation
context
Finally,
on
were
attenuated
transfection
(HSPA1L-K130R)
mutant
plasmid
vitro.
These
findings
indicated
alleviated
promoting
PARKIN-dependent
pathway
via
regulating
site
PTCs,
provided
a
mechanistic
basis
therapeutic
target
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(13), P. 10420 - 10420
Published: June 21, 2023
Mitochondria
play
a
key
role
in
cancer
and
their
involvement
is
not
limited
to
the
production
of
ATP
only.
also
produce
reactive
oxygen
species
building
blocks
sustain
rapid
cell
proliferation;
thus,
deregulation
mitochondrial
function
associated
with
disease
development
progression.
In
cells,
metabolic
reprogramming
takes
place
through
different
modulation
pathways,
including
oxidative
phosphorylation,
fatty
acid
oxidation,
Krebs
cycle,
glutamine
heme
metabolism.
Alterations
homeostasis,
particular,
biogenesis,
mitophagy,
dynamics,
redox
balance,
protein
were
observed
cells.
The
use
drugs
acting
on
destabilization
may
represent
promising
therapeutic
approach
tumors
which
respiration
predominant
energy
source.
this
review,
we
summarize
main
features
pathways
altered
moreover,
present
best
known
that,
by
homeostasis
induce
alterations
death.
addition,
new
strategies
that
damage,
such
as
photodynamic,
photothermal
chemodynamic
therapies,
nanoformulations
specifically
target
mitochondria
are
described.
Thus,
mitochondria-targeted
open
frontiers
tailored
personalized
therapy.
