Unraveling the causes of sarcopenia: Roles of neuromuscular junction impairment and mitochondrial dysfunction
Yanmei Miao,
No information about this author
Leiyu Xie,
No information about this author
Jiamei Song
No information about this author
et al.
Physiological Reports,
Journal Year:
2024,
Volume and Issue:
12(1)
Published: Jan. 1, 2024
Abstract
Sarcopenia
is
a
systemic
skeletal
muscle
disease
characterized
by
decline
in
mass
and
function.
Originally
defined
as
an
age‐associated
condition,
sarcopenia
presently
also
encompasses
muscular
atrophy
due
to
various
pathological
factors,
such
intensive
care
unit‐acquired
weakness,
inactivity,
malnutrition.
The
exact
pathogenesis
of
still
unknown;
herein,
we
review
the
roles
neuromuscular
junction
mitochondria
this
condition.
caused
complex
interdependent
pathophysiological
mechanisms,
including
aging,
impairment,
mitochondrial
dysfunction,
insulin
resistance,
lipotoxicity,
endocrine
oxidative
stress,
inflammation.
Among
these,
instability
dysfunction
are
particularly
significant.
Dysfunction
can
lead
weakness
or
paralysis.
Mitochondria,
which
plentiful
neurons
fibers,
play
important
role
transmission.
Therefore,
impairments
both
may
be
one
key
mechanisms
leading
sarcopenia.
Moreover,
article
explores
structural
functional
alterations
sarcopenia,
suggesting
that
deeper
understanding
these
changes
could
provide
valuable
insights
for
prevention
treatment
Language: Английский
Physiological mechanisms of neuromuscular impairment in diabetes‐related complications: Can physical exercise help prevent it?
Edoardo Lecce,
No information about this author
Alessio Bellini,
No information about this author
Giuseppe Greco
No information about this author
et al.
The Journal of Physiology,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 3, 2025
Diabetes
mellitus
is
a
chronic
disorder
that
progressively
induces
complications,
compromising
daily
independence.
Among
these,
diabetic
neuropathy
particularly
prevalent
and
contributes
to
substantial
neuromuscular
impairments
in
both
types
1
2
diabetes.
This
condition
leads
structural
damage
affecting
the
central
peripheral
nervous
systems,
resulting
significant
decline
sensorimotor
functions.
Alongside
neuropathy,
myopathy
also
muscle
impairment
reduced
motor
performance,
intensifying
decline.
Diabetic
typically
implicates
neurogenic
atrophy,
motoneuron
loss
clustering
of
fibres
as
result
aberrant
denervation-reinervation
processes.
These
complications
are
associated
with
compromised
junctions,
where
alterations
occur
pre-synaptic
vesicles,
mitochondrial
content
post-synaptic
signalling.
Neural
intensified
by
hyperglycaemia
oxidative
stress,
exacerbating
vascular
dysfunction
reducing
oxygen
delivery.
imply
severe
evidenced
reductions
maximal
force
power
output,
rate
development
endurance.
Furthermore,
diabetes-related
compounded
age-related
degenerative
changes
long-term
patients.
Aerobic
resistance
training
offer
promising
approaches
for
managing
blood
glucose
levels
function.
exercise
promotes
biogenesis
angiogenesis,
supporting
metabolic
cardiovascular
health.
Resistance
primarily
enhances
neural
plasticity,
strength
hypertrophy,
which
crucial
factors
mitigating
sarcopenia
preserving
functional
topical
review
examines
current
evidence
on
physiological
mechanisms
underlying
potential
impact
physical
activity
counteracting
this
Language: Английский
The Roles of myomiRs in the Pathogenesis of Sarcopenia: From Literature to In Silico Analysis
Huanxia Jia,
No information about this author
Nurgulsim Kaster,
No information about this author
Rajwali Khan
No information about this author
et al.
Molecular Biotechnology,
Journal Year:
2025,
Volume and Issue:
unknown
Published: March 1, 2025
Language: Английский
Sarcopenia as a Risk Factor for Alzheimer’s Disease: Genetic and Epigenetic Perspectives
Genes,
Journal Year:
2024,
Volume and Issue:
15(5), P. 561 - 561
Published: April 27, 2024
Sarcopenia,
defined
as
the
age-associated
loss
of
muscle
mass
and
increased
fragility
with
age,
is
increasing
worldwide.
The
condition
often
precedes
development
Alzheimer’s
disease,
thereby
decreasing
levels
mobility
physical
activity
in
those
affected.
Indeed,
has,
some
studies,
been
associated
an
risk
disease
other
dementias.
However,
a
detailed
understanding
interplay
between
both
conditions
not
available
needs
to
be
thoroughly
addressed.
In
following
review,
we
focus
on
several
genes,
specifically
APOE,
BDNF,
ACE,
FTO,
FNDC5,
that
have
conditions.
We
also
discuss
epigenetic
regulation
each
these
genes
along
non-coding
RNAs
(ncRNAs)
may
role
sarcopenic
phenotypes.
Finally,
assert
application
systems
biology
will
unravel
relationship
sarcopenia
believe
prevention
older
age
reduce
incidence
debilitating
cognitive
decline.
Language: Английский
Impact of Ageing and Disuse on Neuromuscular Junction and Mitochondrial Function and Morphology: Current Evidence and Controversies
Ageing Research Reviews,
Journal Year:
2024,
Volume and Issue:
unknown, P. 102586 - 102586
Published: Nov. 1, 2024
Language: Английский
Activating Striatal Parvalbumin Interneurons to Alleviate Chemotherapy‐Induced Muscle Atrophy
Journal of Cachexia Sarcopenia and Muscle,
Journal Year:
2025,
Volume and Issue:
16(2)
Published: April 1, 2025
Language: Английский
Sarcopenia and the biological determinants of aging: A narrative review from a geroscience perspective
Mariá Nunes-Pinto,
No information about this author
Renato Gorga Bandeira de Mello,
No information about this author
M. Pinto
No information about this author
et al.
Ageing Research Reviews,
Journal Year:
2024,
Volume and Issue:
103, P. 102587 - 102587
Published: Nov. 19, 2024
Language: Английский
Accelerated Sarcopenia Phenotype in the DJ-1/Park7-Knockout Zebrafish
Kristine O. Rostad,
No information about this author
Tobias Trognitz,
No information about this author
Ann Kristin Frøyset
No information about this author
et al.
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(12), P. 1509 - 1509
Published: Dec. 11, 2024
Age-dependent
loss
of
muscle
mass
and
function
is
associated
with
oxidative
stress.
DJ-1/
Language: Английский
Proteomic reference map for sarcopenia research: mass spectrometric identification of key muscle proteins of organelles, cellular signaling, bioenergetic metabolism and molecular chaperoning
European Journal of Translational Myology,
Journal Year:
2024,
Volume and Issue:
unknown
Published: May 24, 2024
During
the
natural
aging
process,
frailty
is
often
associated
with
abnormal
muscular
performance.
Although
inter-individual
differences
exit,
in
most
elderly
tissue
mass
and
physiological
functionality
of
voluntary
muscles
drastically
decreases.
In
order
to
study
age-related
contractile
decline,
animal
model
research
central
importance
field
biogerontology.
Here
we
have
analyzed
wild
type
mouse
muscle
establish
a
proteomic
map
crude
extracts.
Proteomics
an
advanced
large-scale
biochemical
method
that
attempts
identify
all
accessible
proteins
given
biological
sample.
It
technology-driven
approach
uses
spectrometry
for
characterization
individual
protein
species.
Total
extracts
were
used
this
minimize
potential
introduction
artefacts
due
excess
subcellular
fractionation
procedures.
report,
survey
aged
has
focused
on
organellar
marker
proteins,
as
well
are
involved
cellular
signaling,
regulation
ion
homeostasis,
bioenergetic
metabolism
molecular
chaperoning.
Hence,
reference
highly
suitable
system
future
research.
Language: Английский
Possible Extracellular Signals to Ameliorate Sarcopenia in Response to Medium-Chain Triglycerides (8:0 and 10:0) in Frail Older Adults
Nutrients,
Journal Year:
2024,
Volume and Issue:
16(16), P. 2606 - 2606
Published: Aug. 8, 2024
In
frail
older
adults
(mean
age
85
years
old),
a
3-month
supplementation
with
low
dose
(6
g/day)
of
medium-chain
triglycerides
(MCTs;
C8:0
and
C10:0)
given
at
meal
increased
muscle
mass
function,
relative
to
long-chain
(LCTs),
but
it
decreased
fat
mass.
The
reduction
in
was
partly
due
postprandial
energy
expenditure
by
stimulation
the
sympathetic
nervous
system
(SNS).
However,
extracellular
signals
ameliorate
sarcopenia
are
unclear.
following
three
potential
increase
function
after
MCT
discussed:
(1)
Activating
SNS-the
hypothesis
for
this
is
based
on
evidence
that
beta2-adrenergic
receptor
agonist
acutely
(1-24
h)
markedly
upregulates
isoforms
peroxisomal
proliferator-activated
gamma
coactivator-1alpha
(PGC-1alpha)
mRNAs,
promotes
mitochondrial
biogenesis,
chronically
(~1
month)
induces
hypertrophy.
(2)
An
concentration
plasma
acyl-ghrelin
stimulates
growth
hormone
secretion.
(3)
A
nitrogen-sparing
effect
ketone
bodies,
which
fuel
skeletal
muscle,
may
promote
protein
synthesis
prevent
breakdown.
This
review
will
help
guide
clinical
trials
using
MCTs
treat
primary
(age-related)
sarcopenia.
Language: Английский