Abstract
Muscle
atrophy,
characterized
by
the
loss
of
muscle
mass
and
function,
is
a
hallmark
sarcopenia
cachexia,
frequently
associated
with
aging,
malignant
tumors,
chronic
heart
failure,
malnutrition.
Moreover,
it
poses
significant
challenges
to
human
health,
leading
increased
frailty,
reduced
quality
life,
heightened
mortality
risks.
Despite
extensive
research
on
consensus
in
their
assessment
remains
elusive,
inconsistent
conclusions
regarding
molecular
mechanisms.
atrophy
models
are
crucial
tools
for
advancing
this
field.
Currently,
animal
used
clinical
basic
scientific
studies
induced
through
various
methods,
including
genetic
editing,
nutritional
modification,
exercise,
wasting
diseases,
drug
administration.
also
include
vitro
small
organism
models.
value,
each
these
has
certain
limitations.
This
review
focuses
limitations
diverse
applications
understand
encourage
rational
use
future
research,
therefore
deepening
understanding
underlying
pathophysiological
mechanisms,
ultimately
exploration
therapeutic
strategies
cachexia.
Stem Cell Research & Therapy,
Journal Year:
2025,
Volume and Issue:
16(1)
Published: Feb. 4, 2025
Muscle
disuse
and
offloading
in
microgravity
are
likely
the
primary
factors
mediating
spaceflight-induced
muscle
atrophy,
for
which
there
is
currently
no
effective
treatment
other
than
exercise.
Extracellular
vesicles
derived
from
bone
marrow
mesenchymal
stem
cells
(BMSC-EVs)
possess
anti-inflammatory
antioxidant
properties,
offering
a
potential
strategy
combating
weightless
muscular
atrophy.
In
this
study,
human
BMSCs-EVs
(hBMSC-EVs)
were
isolated
using
super-centrifugation
characterized.
C2C12
myotube
nutrition-deprivation
mice
tail
suspension
models
established.
Subsequently,
diameter
of
myotubes,
Soleus
mass,
cross-sectional
area
(CSA)
fibers,
grip
strength
assessed
to
investigate
impact
hBMSC-EVs
on
Immunostaining,
transmission
electron
microscopy
observation,
western
blot
analysis
employed
assess
fiber
types,
ROS
levels,
inflammation,
ubiquitin–proteasome
system
activity,
autophagy
lysosome
pathway
activation
skeletal
The
active
can
be
internalized
by
myotubes
muscle.
effectively
reduce
atrophy
caused
nutritional
deprivation,
with
concentration
10
×
108
particles/mL
showing
best
effect
(P
<
0.001).
Additionally,
down-regulate
protein
levels
associated
UPS
oxidative
stress.
Moreover,
intravenous
administration
at
1
1010
reverse
reduction
soleus
mass
0.001),
CSA
0.01),
0.001)
weightlessness.
They
demonstrate
ability
inhibit
degradation
mediated
pathway,
along
suppression
stress
inflammatory
responses.
Furthermore,
impede
transition
slow
fibers
fast
via
upregulation
Sirt1
PGC-1α
levels.
Our
findings
indicate
that
capable
inhibiting
excessive
suppressing
response,
reversing
type
transformation,
delaying
hindlimb
unloading-induced
enhancing
function.
study
has
further
advanced
understanding
molecular
mechanism
underlying
weightlessness
demonstrated
protective
Deleted Journal,
Journal Year:
2025,
Volume and Issue:
2(1)
Published: March 28, 2025
Abstract
Background
Hyperbaric
hyperoxia
exposure
improves
skeletal
muscle
capillary
rarefaction
and
mitochondrial
activity
in
diabetes
mellitus
(DM).
However,
the
hyperbaric
environment
is
limited,
normobaric
effects
on
capillaries
DM
are
unknown.
We
determined
density
type
1
rats.
Methods
Seven-week-old
male
Wistar
rats
were
randomly
divided
into
control,
DM,
with
40%
oxygen
(DM40),
50%
(DM50)
groups.
A
single
intraperitoneal
injection
of
streptozotocin
was
administered
to
induce
DM.
DM40
DM50
exposures
conducted
daily
for
60
min
4
weeks.
The
soleus
muscle,
extensor
digitorum
longus
plantaris
samples
sectioned.
capillary-to-fiber
ratio
measured
using
alkaline
phosphatase
staining.
Succinate
dehydrogenase
(SDH)
by
SDH
Scheffe’s
test
performed
multiple
comparisons,
Pearson’s
correlation
coefficients
between
calculated.
Statistical
significance
set
at
<
5%.
Results
muscles
significantly
higher
than
(all
p
0.01).
Moreover,
rats;
same
found
significant
positive
observed
0.05).
Conclusions
Normobaric
affected
all
muscles,
reflecting
their
fiber
characteristics.
Skeletal
associated
activity,
suggesting
improved
metabolism.
Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
15
Published: Oct. 14, 2024
Introduction
Diabetic
ketoacidosis
(DKA)
is
a
severe
and
potentially
fatal
acute
complication
in
diabetic
patients,
commonly
occurring
type
1
diabetes
(T1D)
but
also
seen
2
(T2D).
The
pathogenesis
of
DKA
involves
complex
physiological
processes
that
are
not
fully
understood,
especially
the
role
mitochondria.
Mitochondria,
known
as
powerhouse
cells,
plays
crucial
oxidative
phosphorylation
ATP
production,
which
vital
various
metabolic
diseases,
including
diabetes.
However,
exact
causal
relationship
between
mitochondrial
dysfunction
remains
unclear.
Methods
This
study
employed
Mendelian
randomization
(MR)
analysis
protein-protein
interaction
(PPI)
networks
to
systematically
explore
relationships
DNA
copy
number
(mtDNA-CN)
specific
proteins
with
DKA.
We
used
bidirectional
MR
genome-wide
association
(GWAS)
data
from
openGWAS
database
investigate
effects
mtDNA-CN
64
mitochondrial-related
on
its
subtypes
(T1DKA,
T2DKA,
unspecified-DKA).
Results
revealed
increased
significantly
reduces
risk
DKA,
whereas
effect
was
significant.
Mitochondrial-related
such
MRPL32,
MRPL33,
COX5B,
DNAJC19,
NDUFB8
showed
negative
indicating
their
potential
protective
roles.
Conversely,
ATP5F1B
COX4I2
have
positive
excessive
production
patients
may
be
detrimental
health
increase
complications
Discussion
results
emphasize
necessity
protecting
function
order
reduce
offers
novel
perspectives
molecular
pathways
involved
emphasizing
critical
functions
mt-DNA
distinct
proteins.
These
evidences
only
enhance
our
comprehension
implications
diabetes-related
identify
therapeutic
targets
for
individualized
treatment
approaches,
thereby
making
substantial
contribution
clinical
care
public
initiatives.
Immunity & Ageing,
Journal Year:
2024,
Volume and Issue:
21(1)
Published: Aug. 5, 2024
Sarcopenia
is
a
complex
age-associated
syndrome
of
progressive
loss
muscle
mass
and
strength.
Although
this
condition
influenced
by
many
factors,
age-related
changes
in
immune
function
including
cell
dynamics,
chronic
inflammation
contribute
to
its
progression.
The
interplay
between
the
system,
gut-muscle
axis,
autophagy
further
underscores
their
important
roles
sarcopenia
pathogenesis.
Immunomodulation
has
emerged
as
promising
strategy
counteract
sarcopenia.
Traditional
management
approaches
treat
physical
exercise
nutritional
supplementation,
emerging
technologies
biophysical
stimulation
demonstrated
importance
immunomodulation
regulation
macrophages
T
cells
reduction
inflammation.
Treatments
alleviate
low-grade
older
adults
modulating
gut
microbial
composition
diversity
combat
Furthermore,
some
pharmacological
interventions,
nano-medicine,
therapies
targeting
muscle,
microbiota,
or
present
additional
avenues
for
This
narrative
review
explores
immunological
underpinnings
sarcopenia,
elucidating
relationship
system
during
ageing.
Additionally,
discusses
new
areas
such
axis
autophagy,
which
bridge
health.
Insights
into
current
potential
through
modulation
are
provided,
along
with
suggestions
future
research
directions
therapeutic
strategies.
We
aim
guide
investigation
clinical
biomarkers
identify
indicators
diagnosis
treatment
targets
condition.
also
draw
attention
considering
Critical Reviews in Food Science and Nutrition,
Journal Year:
2024,
Volume and Issue:
unknown, P. 1 - 17
Published: July 25, 2024
Diabetes
has
become
a
serious
public
health
crisis,
presenting
significant
challenges
to
individuals
worldwide.
As
the
largest
organ
in
human
body,
skeletal
muscle
is
target
of
this
chronic
disease,
yet
wasting
as
complication
diabetes
still
not
fully
understood
and
effective
treatment
methods
have
be
developed.
Here,
we
discuss
targets
involved
inducing
under
diabetic
conditions,
both
validated
emerging
targets.
Diabetes-induced
known
involve
changes
various
signaling
molecules
pathways,
such
protein
degradation
synthesis
mitochondrial
function,
oxidative
stress
inflammation.
Recent
studies
shown
that
some
these
present
potential
promising
therapeutic
targets,
including
neuregulin
1/epidermal
growth
factor
receptor
family,
advanced
glycation
end-products,
irisin,
ferroptosis,
differentiation
15
more.
This
study's
investigation
discussion
pathways
their
applications
provides
theoretical
basis
for
development
clinical
treatments
diabetes-induced
foundation
continued
focus
on
disease.
International Journal of Medical Arts,
Journal Year:
2024,
Volume and Issue:
0(0), P. 0 - 0
Published: July 9, 2024
Background:
Diabetes
mellitus
and
other
chronic
medical
conditions
are
associated
with
ageing.
Sarcopenia
is
also
affected
elderly
populations.
The
role
of
inflammation
oxidative
stress
in
both
poorly
investigated.The
aim
the
work:
current
work
was
designed
to
examine
possible
association
sarcopenia
diabetes
subjects.
Patients
Methods:
Eighty
patients
older
than
65
years
age
were
included
work.
They
categorized
into
two
equal
groups;
first
for
second
diabetics
without
sarcopenia.
All
clinically
evaluated,
addition
laboratory
workup
check
oxidant-antioxidant
system
besides
some
inflammatory
markers.Results:
No
significant
differences
recognized
regarding
patient
demographics,
comorbid
or
duration
diabetes.
There
reduction
BMI,
hip
circumference,
skeletal
muscle
mass
gait
speed
sarcopenic
non-sarcopenic
group
[25.51
±
0.67,
98.15
3.97,
7.07
0.83
0.68
0.11
vs.
27.07
1.31,
105.53
4.59,
9.44
1.01
0.98
0.12,
successively].
increase
CRP,
xanthine
oxidase,
groups
[5.15
0.72,
0.532
0.109
3.03
0.78,
0.344
0.063,
respectively].
However,
plasma
glutathione
significantly
reduced
[0.190±0.057
0.233±0.047,
Finally,
glutathione,
BMI
absolute
development
sarcopenia.Conclusion:
Oxidative
disturbance
systems
seems
play
a
crucial
