AMPK signaling is dysregulated in human tendinopathy and loss of AMPKα1 leads to cell, matrix and mechanical dysfunction in mouse Achilles tendon
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2025,
Номер
unknown
Опубликована: Фев. 1, 2025
SUMMARY
Tendinopathy
is
a
tendon
disorder
that
caused
by
the
failure
to
self-repair
and
has
many
pathological
characteristics
such
as
disorganized
ECM
decreased
cell
viability.
We
have
identified
possible
target
combat
these
changes,
AMPK,
an
energy
stress
sensor
was
shown
maintain
intracellular
homeostasis.
Through
bulk
RNA-sequencing
of
healthy
tendinopathic
tendons
from
humans
we
novel
finding
downregulation
AMPK
signaling
in
samples
which
suggests
plays
role
Our
studies
utilizing
conditional
knock-out
Prkaa1
mice
showed
loss
results
degenerative
ECM,
impaired
biomechanical
properties
increased
cellular
senescence
Achilles
through
lifespan.
Additionally,
found
exercise
can
delay
onset
independent
AMPK.
These
findings
highlight
importance
metabolism
health
will
assist
understanding
progression
tendinopathy.
Язык: Английский
Bone Adaptations to a Whole Body Vibration Protocol in Murine Models of Different Ages: A Preliminary Study on Structural Changes and Biomarker Evaluation
Journal of Functional Morphology and Kinesiology,
Год журнала:
2025,
Номер
10(1), С. 26 - 26
Опубликована: Янв. 10, 2025
Background/Objectives:
Whole
body
vibration
(WBV)
is
a
valuable
tool
to
mitigate
physiological
adaptations
related
age
and
inactivity.
Although
significant
benefits
have
been
found
at
the
musculoskeletal
level,
including
increased
bone
mass
reduced
muscle
atrophy,
underlying
biological
mechanisms
remain
largely
unknown.
Therefore,
our
study
aimed
evaluate
effects
of
vibratory
training
on
tissue
in
murine
models
different
groups
by
investigating
structural
distribution
changes
some
crucial
biomarkers
involved
homeostasis.
Methods:
Specifically,
4-,
12-,
24-month-old
mice
were
trained
with
WBV
protocol
characterized
three
series
2
min
30
s,
interspersed
recovery
period
same
duration,
3-weekly
frequency
for
3
months.
At
end
training,
histological
morphometric
analyses
conducted,
association
immunohistochemical
analysis
investigate
fibronectin
type
III
domain-containing
protein
5
(FNDC5),
NADPH
oxidase
4
(NOX4),
sirtuin
1
(SIRT1).
Results:
Our
preliminary
results
showed
that
improves
health
preserving
architecture
promoting
up-regulation
FNDC5
SIRT1
down-regulation
NOX4.
Conclusions:
confirms
as
viable
alternative
counter
decline
elderly
and/or
sedentary
subjects.
Further
investigations
should
be
conducted
deepen
knowledge
this
field
explore
role
other
molecular
mediators
vibration.
Язык: Английский
SIRT1 and exercise-induced bone metabolism: a regulatory nexus
Frontiers in Cell and Developmental Biology,
Год журнала:
2025,
Номер
13
Опубликована: Март 26, 2025
Regular
exercise
positively
influences
bone
health,
enhances
density
and
strength,
reduces
the
risk
of
osteoporosis.
Silent
information
regulator
transcription
1
(SIRT1)
is
a
deacetylase
that
plays
pivotal
role
in
regulation
various
biological
processes.
In
this
review,
we
explore
SIRT1
modulating
metabolism
response
to
exercise.
regulates
crucial
cellular
processes,
including
inflammation,
aging,
autophagy,
oxidative
stress,
cells
such
as
marrow
mesenchymal
stem
cells,
osteoblasts,
osteoclasts,
exercise-induced
stimuli.
Notably,
by
muscle
neurotransmitters,
with
acting
key
mediator.
A
comprehensive
understanding
SIRT1’s
regulatory
mechanisms
will
facilitate
deeper
exploration
principles
underlying
improvements
metabolism,
ultimately
providing
novel
insights
into
treatment
metabolic
disorders.
Язык: Английский