Journal of Nanobiotechnology,
Год журнала:
2024,
Номер
22(1)
Опубликована: Авг. 14, 2024
Mitochondria
are
crucial
organelles
responsible
for
energy
generation
in
eukaryotic
cells.
Oxidative
stress,
calcium
disorders,
and
mitochondrial
DNA
abnormalities
can
all
cause
dysfunction.
It
is
now
well
documented
that
dysfunction
significantly
contributes
to
the
pathogenesis
of
numerous
illnesses.
Hence,
it
vital
investigate
innovative
treatment
methods
targeting
Extracellular
vesicles
(EVs)
cell-derived
nanovesicles
serve
as
intercellular
messengers
classified
into
small
EVs
(sEVs,
<
200
nm)
large
(lEVs,
>
based
on
their
sizes.
worth
noting
certain
subtypes
rich
components
(even
structurally
intact
mitochondria)
possess
ability
transfer
them
or
other
contents
including
proteins
nucleic
acids
recipient
cells
modulate
function.
Specifically,
target
cell
homeostasis
mitochondria-controlled
apoptosis
ROS
by
delivering
relevant
substances.
In
addition,
artificial
modification
delivery
carriers
therapeutic
goods
mitochondria
also
a
current
research
hotspot.
this
article,
we
will
focus
function
cells,
aiming
offer
novel
perspectives
approaches
diverse
conditions
linked
Redox Biology,
Год журнала:
2024,
Номер
74, С. 103224 - 103224
Опубликована: Июнь 8, 2024
Silicosis,
characterized
by
interstitial
lung
inflammation
and
fibrosis,
poses
a
significant
health
threat.
ATII
cells
play
crucial
role
in
alveolar
epithelial
repair
structural
integrity
maintenance.
Inhibiting
cell
senescence
has
shown
promise
silicosis
treatment.
However,
the
mechanism
behind
silica-induced
remains
elusive.
The
study
employed
male
C57BL/6
N
mice
A549
human
to
investigate
its
potential
Silicosis
was
induced
via
intratracheal
instillation
of
crystalline
silica
particles,
with
honokiol
administered
intraperitoneally
for
14
days.
Silica-induced
confirmed,
SIRT3
knockout
overexpression
lines
were
generated.
Various
analyses
conducted,
including
immunoblotting,
qRT-PCR,
histology,
transmission
electron
microscopy.
Statistical
significance
determined
using
one-way
ANOVA
Tukey's
post-hoc
test.
This
elucidates
how
induces
senescence,
emphasizing
mtDNA
damage.
Notably,
(HKL)
emerges
as
promising
anti-senescence
anti-fibrosis
agent,
acting
through
sirt3.
effectively
attenuated
cells,
dependent
on
sirt3
expression,
while
mitigating
Sirt3,
class
III
histone
deacetylase,
regulates
mitochondrial
stress.
HKL
activates
sirt3,
protecting
against
pulmonary
fibrosis
Additionally,
downregulated
cGAS
expression
senescent
silica,
suggesting
sirt3's
an
upstream
regulator
cGAS/STING
signaling
pathway.
Moreover,
treatment
inhibited
activation
NF-κB
pathway,
associated
reduced
oxidative
stress
enhanced
activity
SOD2,
function,
sirt3-mediated
deacetylation.
promoted
deacetylation
further
safeguarding
integrity.
uncovers
natural
compound,
HKL,
anti-fibrotic
properties
activating
shedding
light
pathogenesis
avenues.
Frontiers in Pharmacology,
Год журнала:
2025,
Номер
15
Опубликована: Янв. 3, 2025
Chronic
obstructive
pulmonary
disease
(COPD)
is
a
prevalent
chronic
respiratory
worldwide.
Mitochondrial
quality
control
mechanisms
encompass
processes
such
as
mitochondrial
biogenesis,
fusion,
fission,
and
autophagy,
which
collectively
maintain
the
quantity,
morphology,
function
of
mitochondria,
ensuring
cellular
energy
supply
progression
normal
physiological
activities.
However,
in
COPD,
due
to
persistent
stimulation
harmful
factors
smoking
air
pollution,
often
become
deregulated,
leading
dysfunction.
dysfunction
plays
pivotal
role
pathogenesis
contributing
toinflammatory
response,
oxidative
stress,
senescence.
therapeutic
strategies
targeting
mitochondria
remain
underexplored.
This
review
highlights
recent
advances
focusing
on
their
dysregulation
progression.
We
emphasize
significance
pathophysiological
COPD
explore
potential
regulate
improve
through
interventions,
aiming
treat
effectively.
Additionally,
we
analyze
limitations
challenges
existing
strategies,
provide
new
insights
methods
for
treatment.
Frontiers in Aging Neuroscience,
Год журнала:
2025,
Номер
16
Опубликована: Фев. 12, 2025
Peroxisome
proliferator-activated
receptor-
γ
coactivator-1α
(PGC-1α),
which
is
highly
expressed
in
the
central
nervous
system,
known
to
be
involved
regulation
of
mitochondrial
biosynthesis,
metabolic
regulation,
neuroinflammation,
autophagy,
and
oxidative
stress.
This
knowledge
indicates
a
potential
role
PGC-1α
wide
range
functions
associated
with
neurological
diseases.
There
emerging
evidence
indicating
protective
pathogenesis
several
As
such,
deeper
broader
understanding
its
diseases
urgently
needed.
The
present
review
provides
relatively
complete
overview
current
on
PGC-1α,
including
different
types
neurons,
basic
structural
characteristics,
interacting
transcription
factors.
Furthermore,
we
various
diseases,
such
as
intracerebral
hemorrhage,
ischemic
stroke,
Alzheimer’s
disease,
Parkinson’s
Amyotrophic
lateral
sclerosis,
Huntington’s
other
PolyQ
Importantly,
discuss
some
compounds
or
drug-targeting
strategies
that
have
been
studied
ameliorate
pathology
these
introduce
possible
mechanistic
pathways.
Based
available
studies,
propose
targeting
could
serve
promising
novel
therapeutic
strategy
for
one
more
Abstract
The
silencing
regulatory
factor
2-like
protein
3
(SIRT3)
is
a
nicotinamide
adenine
dinucleotide
(NAD+)
dependent
deacetylase
located
primarily
in
the
mitochondria.
This
plays
an
important
role
oxidative
stress,
energy
metabolism,
and
autophagy
multicellular
organisms.
Autophagy
(macroautophagy)
cytoprotective
mechanism
necessary
for
intracellular
homeostasis
synthesis,
degradation,
recycling
of
cellular
products.
can
influence
progression
several
neural,
cardiac,
hepatic,
renal
diseases
also
contribute
to
development
fibrosis,
diabetes,
many
types
cancer.
Recent
studies
have
shown
that
SIRT3
has
regulating
autophagy.
Therefore
this
study,
we
aimed
perform
literature
review
summarize
regulation
findings
study
could
be
used
identify
new
drug
targets
SIRT3-related
diseases.
Methods
:
A
comprehensive
involved
behind
autophagy-related
was
performed.
Relevant
published
Pubmed
Web
Science
up
July
2023
identified
using
keywords
“silencing
3”,
“SIRT3”
“autophagy”.
