Nature,
Год журнала:
2022,
Номер
613(7942), С. 169 - 178
Опубликована: Дек. 21, 2022
Abstract
Tissue
regeneration
requires
coordination
between
resident
stem
cells
and
local
niche
1,2
.
Here
we
identify
that
senescent
are
integral
components
of
the
skeletal
muscle
regenerative
repress
at
all
stages
life.
The
technical
limitation
senescent-cell
scarcity
3
was
overcome
by
combining
single-cell
transcriptomics
a
enrichment
sorting
protocol.
We
identified
isolated
different
cell
types
from
damaged
muscles
young
old
mice.
Deeper
transcriptome,
chromatin
pathway
analyses
revealed
conservation
identity
traits
as
well
two
universal
senescence
hallmarks
(inflammation
fibrosis)
across
type,
time
ageing.
Senescent
create
an
aged-like
inflamed
mirrors
inflammation
associated
with
ageing
(inflammageing
4
)
arrests
proliferation
regeneration.
Reducing
burden
cells,
or
reducing
their
inflammatory
secretome
through
CD36
neutralization,
accelerates
in
By
contrast,
transplantation
delays
Our
results
provide
technique
for
isolating
vivo
define
blueprint
muscle,
uncover
unproductive
functional
interactions
niches
can
be
overcome.
As
also
accumulate
human
muscles,
our
findings
open
potential
paths
improving
repair
throughout
Metabolism,
Год журнала:
2023,
Номер
146, С. 155639 - 155639
Опубликована: Июнь 27, 2023
Sarcopenic
obesity,
or
the
loss
of
muscle
mass
and
function
associated
with
excess
adiposity,
is
a
largely
untreatable
medical
condition
diminished
quality
life
increased
risk
mortality.
To
date,
it
remains
somewhat
paradoxical
mechanistically
undefined
as
to
why
subset
adults
obesity
develop
muscular
decline,
an
anabolic
stimulus
generally
retention
lean
mass.
Here,
we
review
evidence
surrounding
definition,
etiology,
treatment
sarcopenic
emphasis
on
emerging
regulatory
nodes
therapeutic
potential.
We
available
clinical
focused
diet,
lifestyle,
behavioral
interventions
improve
in
patients
obesity.
Based
upon
evidence,
relieving
consequences
energy
burden,
such
oxidative
stress,
myosteatosis,
and/or
mitochondrial
dysfunction,
promising
area
for
development
management
Phytotherapy Research,
Год журнала:
2024,
Номер
38(5), С. 2496 - 2517
Опубликована: Март 6, 2024
Abstract
We
investigated
the
mechanism
by
which
quercetin
preserves
mitochondrial
quality
control
(MQC)
in
cardiomyocytes
subjected
to
ischemia–reperfusion
stress.
An
enzyme‐linked
immunosorbent
assay
was
employed
vivo
experiments
assess
myocardial
injury
markers,
measure
transcript
levels
of
SIRT5/DNAPK‐cs/MLKL
during
various
time
intervals
ischemia–reperfusion,
and
observe
structural
changes
using
transmission
electron
microscopy.
In
vitro
investigations,
adenovirus
transfection
establish
a
gene‐modified
model
DNA‐PKcs,
primary
were
obtained
from
mouse
with
modified
SIRT5
gene.
Reverse
transcription
polymerase
chain
reaction,
laser
confocal
microscopy,
immunofluorescence
localization,
JC‐1
fluorescence
assay,
Seahorse
energy
analysis,
other
assays
applied
corroborate
regulatory
influence
on
MQC
network
after
ischemia–reperfusion.
demonstrated
that
caused
structure
myocardium.
It
seen
had
beneficial
effect
tissue,
providing
protection.
As
process
continued,
DNA‐PKcs/SIRT5/MLKL
transcripts
also
found
change.
investigations
revealed
mitigated
cardiomyocyte
oxidative
stress
through
regulated
mitophagy
kinetics
sustain
optimal
metabolism
levels.
Quercetin,
desuccinylation,
modulated
stability
together
they
“mitophagy‐unfolded
protein
response.”
This
preserved
integrity
membrane
genome,
dynamics,
metabolism.
Quercetin
may
operate
synergistically
oversee
regulation
unfolded
response
DNA‐PKcs‐SIRT5
interaction.
Cellular & Molecular Biology Letters,
Год журнала:
2024,
Номер
29(1)
Опубликована: Март 4, 2024
Acute
kidney
injury
(AKI)
is
a
common
clinical
disorder
with
complex
etiology
and
poor
prognosis,
currently
lacks
specific
effective
treatment
options.
Mitochondrial
dynamics
dysfunction
prominent
feature
in
AKI,
modulation
of
mitochondrial
morphology
may
serve
as
potential
therapeutic
approach
for
AKI.
Aging
skin,
vulnerable
to
age-related
defects,
is
poor
in
wound
repair.
Metabolic
regulation
accumulated
senescent
cells
(SnCs)
with
aging
essential
for
tissue
homeostasis,
and
adequate
ATP
important
cell
activation
aged
Strategies
metabolism
intervention
hold
prospects
therapeutic
advances.
Here,
we
found
energy
metabolic
changes
skin
from
patients
mice.
Our
data
show
that
metformin
engineered
EV
(Met-EV)
can
enhance
mouse
repair,
as
well
ameliorate
cellular
senescence
restore
dysfunctions.
Notably,
was
remodeled
reduced
glycolysis
enhanced
OXPHOS
after
Met-EV
treatment.
We
rescue
senescence-induced
mitochondria
dysfunctions
mitophagy
suppressions,
indicating
the
role
of
remodeling
mitochondrial
functions
via
production
results
reveal
mechanism
SnCs
rejuvenation
by
suggest
disturbed
metabolism,
be
a
potential
target
facilitating
Nature Cell Biology,
Год журнала:
2024,
Номер
26(12), С. 2046 - 2060
Опубликована: Окт. 21, 2024
Tissue-scale
architecture
and
mechanical
properties
instruct
cell
behaviour
under
physiological
diseased
conditions,
but
our
understanding
of
the
underlying
mechanisms
remains
fragmentary.
Here
we
show
that
extracellular
matrix
stiffness,
spatial
confinements
applied
forces,
including
stretching
mouse
skin,
regulate
mitochondrial
dynamics.
Actomyosin
tension
promotes
phosphorylation
elongation
factor
1
(MIEF1),
limiting
recruitment
dynamin-related
protein
(DRP1)
at
mitochondria,
as
well
peri-mitochondrial
F-actin
formation
fission.
Strikingly,
fission
is
also
a
general
mechanotransduction
mechanism.
Indeed,
found
DRP1-
MIEF1/2-dependent
required
sufficient
to
three
transcription
factors
broad
relevance-YAP/TAZ,
SREBP1/2
NRF2-to
control
proliferation,
lipogenesis,
antioxidant
metabolism,
chemotherapy
resistance
adipocyte
differentiation
in
response
cues.
This
extends
liver,
where
DRP1
regulates
hepatocyte
proliferation
identity-hallmark
YAP-dependent
phenotypes.
We
propose
mitochondria
fulfil
unifying
signalling
function
by
which
tissue
microenvironment
coordinates
complementary
functions.
Nature Communications,
Год журнала:
2023,
Номер
14(1)
Опубликована: Сен. 18, 2023
The
use
of
exogenous
mitochondria
to
replenish
damaged
has
been
proposed
as
a
strategy
for
the
treatment
pulmonary
fibrosis.
However,
success
this
is
partially
restricted
by
difficulty
supplying
sufficient
diseased
cells.
Herein,
we
report
generation
high-powered
mesenchymal
stem
cells
with
promoted
mitochondrial
biogenesis
and
facilitated
transfer
injured
lung
sequential
pioglitazone
iron
oxide
nanoparticles.
This
highly
efficient
shown
not
only
restore
homeostasis
but
also
reactivate
inhibited
mitophagy,
consequently
recovering
impaired
cellular
functions.
We
perform
studies
in
mouse
show
that
these
successfully
mitigate
fibrotic
progression
progressive
fibrosis
model,
which
was
further
verified
humanized
multicellular
spheroid
model.
present
findings
provide
potential
overcome
current
limitations
replenishment
therapy,
thereby
promoting
therapeutic
applications
intervention.
Biomedicine & Pharmacotherapy,
Год журнала:
2023,
Номер
165, С. 115147 - 115147
Опубликована: Июль 18, 2023
With
global
population
aging,
age-related
diseases,
especially
sarcopenia,
have
attracted
much
attention
in
recent
years.
Characterized
by
low
muscle
strength,
quantity
or
quality
and
physical
performance,
sarcopenia
is
one
of
the
major
factors
associated
with
an
increased
risk
falls
disability.
Much
effort
has
been
made
to
understand
cellular
biological
physiological
mechanisms
underlying
sarcopenia.
Autophagy
important
self-protection
mechanism
that
relies
on
lysosomes
degrade
misfolded
proteins
damaged
organelles.
Research
designed
obtain
new
insight
into
human
diseases
from
autophagic
aspect
carried
out
progress,
which
encourages
relevant
studies
relationship
between
autophagy
plays
a
protective
role
modulating
regenerative
capability
satellite
cells,
relieving
oxidative
stress
suppressing
inflammatory
response.
This
review
aims
reveal
specific
interaction
explore
possible
therapies
hopes
encouraging
more
research
need
unlocking
novel
promising
ameliorate
