Research Square (Research Square),
Journal Year:
2024,
Volume and Issue:
unknown
Published: Dec. 2, 2024
Abstract
Background
Sarcopenia
is
one
of
the
syndromes
that
cause
falls,
fractures,
and
morbidity
in
geriatric
patients.
Early
diagnosis
sarcopenia
important
as
it
known
muscle
functions
improve
with
early
intervention.
We
aimed
to
investigate
whether
urinary
amino
acid
levels
are
a
biomarker
sarcopenia.
Methods
The
study
included
ninety-one
patients
aged
45–65
who
applied
our
outpatient
clinic.
underwent
physical
examinations,
blood
tests
sixteen
different
urine
were
analyzed.
Anthropometric
measurements
made.
Physical
performances
evaluated.
Muscle
strengths
measured.
masses
Patients
divided
into
4
groups:
pre-sarcopenic,
sarcopenic,
severe
sarcopenic
non-sarcopenic.
Statistical
significance
level
was
determined
p
<
0.05.
Results
A
total
patients,
fifty-three
female
thirty-eight
males,
study.
Three
had
pre-sarcopenia,
eleven
sarcopenia,
two
met
criteria
for
while
seventy-five
non
sarcopenic.
significant
difference
found
between
non-sarcopenia
groups
terms
glutamine
valine
(p
0.001
both).
In
ROC
analysis,
cut-off
value
detecting
492
micromole/L
209
(AUC:0.875;0.968
respectively).
correlation
analysis
strength-mass
negative
leucine
strength
mass.
Conclusions
high
associated
both
Cells,
Journal Year:
2024,
Volume and Issue:
13(3), P. 252 - 252
Published: Jan. 29, 2024
Cachexia
is
a
condition
characterized
by
substantial
loss
of
body
weight
resulting
from
the
depletion
skeletal
muscle
and
adipose
tissue.
A
considerable
fraction
patients
with
advanced
cancer,
particularly
those
who
have
been
diagnosed
pancreatic
or
gastric
lung
prostate
colon
breast
leukemias,
are
impacted
this
condition.
This
syndrome
manifests
at
all
stages
cancer
associated
an
unfavorable
prognosis.
It
heightens
susceptibility
to
surgical
complications,
chemotherapy
toxicity,
functional
impairments,
breathing
difficulties,
fatigue.
The
early
detection
cachexia
has
potential
enhance
both
their
quality
life
overall
survival
rates.
Regarding
matter,
blood
biomarkers,
although
helpful,
possess
certain
limitations
do
not
exhibit
universal
application.
Additionally,
available
treatment
options
for
currently
limited,
there
lack
comprehensive
understanding
underlying
molecular
pathways
Thus,
review
aims
provide
overview
mechanisms
therapeutic
targets
development
effective
treatments
devastating
Cells,
Journal Year:
2023,
Volume and Issue:
12(14), P. 1846 - 1846
Published: July 13, 2023
The
proteasome
is
a
multi-catalytic
protease
complex
that
involved
in
protein
quality
control
via
three
proteolytic
activities
(i.e.,
caspase-,
trypsin-,
and
chymotrypsin-like
activities).
Most
cellular
proteins
are
selectively
degraded
by
the
ubiquitination.
Moreover,
ubiquitin–proteasome
system
critical
process
for
maintaining
homeostasis.
Here,
we
briefly
summarize
structure
of
proteasome,
its
regulatory
mechanisms,
regulate
activity,
alterations
to
activity
found
diverse
diseases,
chemoresistant
cells,
cancer
stem
cells.
Finally,
describe
potential
therapeutic
modalities
use
system.
Bratislavské lekárske listy/Bratislava medical journal,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 29, 2025
Abstract
Background
Sarcopenia
is
a
syndrome
that
cause
falls,
fractures,
and
morbidity
in
geriatric
patients.
Early
diagnosis
of
sarcopenia
important
as
it
known
muscle
functions
can
improve
with
early
intervention.
We
aimed
to
investigate
whether
urinary
amino
acid
levels
could
serve
biomarkers
sarcopenia.
Methods
The
study
included
ninety-one
patients
aged
45–65
who
visited
our
outpatient
clinic.
underwent
physical
examinations,
blood
tests
sixteen
distinct
were
analyzed.
Anthropometric
measurements
performed.
Physical
performances
evaluated.
Muscle
strengths
measured.
masses
Patients
divided
into
4
groups:
pre-sarcopenic,
sarcopenic,
severe
sarcopenic
non-sarcopenic.
Statistical
significance
level
was
determined
p
<
0.05.
Results
A
total
patients,
53
females
38
males,
the
study.
Three
had
pre-sarcopenia,
eleven
sarcopenia,
two
met
criteria
for
while
seventy-five
non
sarcopenic.
significant
difference
found
between
non-sarcopenia
groups
terms
glutamine
valine
(p
0.001
both).
In
ROC
analysis,
cut-off
value
detecting
492
µmol/L
209
(AUC:
0.875
0.968).
Correlation
analysis
revealed
negative
relationship
leucine
both
strength
mass
Conclusions
high
associated
mass.
Journal of Cachexia Sarcopenia and Muscle,
Journal Year:
2025,
Volume and Issue:
16(2)
Published: April 1, 2025
Abstract
Background
Cachexia
is
a
severe
form
of
muscle
wasting
disorder
particularly
observed
in
patients
with
advanced
cancer.
The
absence
effective
strategies
to
ameliorate
cachexia
indicates
our
poor
understanding
the
mechanisms
cachexia.
By
employing
system‐wide
approaches,
we
investigated
molecular
underlying
cancer
secreted
pro‐inflammatory
cytokine‐induced
(CIC).
Methods
As
cellular
model
systems,
employed
mouse
satellite
stem
cell‐derived
primary
cells,
C2C12
myoblast
progenitor
myotubes,
and
neonatal
rat
cardiomyocytes.
We
induced
CIC
by
incubating
striated
cells
cytokines
TNF‐α
IFN‐γ.
To
understand
physiological
effects
CIC,
probed
contractile
properties
following
electrical
stimulation
measured
intracellular
calcium
transients.
Effects
on
sarcomere
organization
were
monitored
confocal
microscopy.
Large‐scale
quantitative
proteomics
RNA
sequencing
assays
enabled
us
examine
CIC.
Using
chromatin
immunoprecipitation
experiments,
signalling
modulation
epigenetic
marks
muscle‐specific
genes
investigated.
Results
Here,
drastic
loss
cell
contraction
primarily,
due
acutely
disorganized
structures
impeded
handling
process.
In
transients,
extent
(Ca
2+
)
release,
as
indicated
amplitude
during
excitation–contraction
coupling
(ECC)
process,
was
reduced
(19.6
±
2.35%
control
8.6
1.52%
p
=
4.8
*
10
−11
).
Kinetics
i.e.,
Ca
release
rate
(26
0.5
ms
29
5.1
median
0.014),
re‐uptake
(137
13
185
24
0.032)
both
prolonged.
Proteomic
analysis
showed
altered
proteostasis
related
sarcoplasmic
reticulum
(SR).
Transcriptomic
unravelled
upstream
deregulation
global
transcriptional
events
for
sarcomeric
SR
genes.
Mechanistically,
loading
transcriptionally
active
Polymerase
II
genes,
including
Myh1
Atp2a1
,
impeded.
This
diminished
H3K4
trimethylation
resulted
lower
activity
these
ultimately
MyHC‐IId
motor
protein
SERCA1
levels.
Conclusions
Our
top‐down
approach
elucidated
that
mechanism
proteomic
state
perturbed
functionally
machinery
responsible
Knowledge
cause
mass
compromised
function
key
developing
therapeutic
solutions
cachectic
conditions.
Foods,
Journal Year:
2024,
Volume and Issue:
13(6), P. 919 - 919
Published: March 18, 2024
Dietary
protein
supplementation
has
emerged
as
a
promising
strategy
in
combating
sarcopenia.
Furthermore,
searching
for
alternatives
of
animal
proteins
been
hot
topic.
The
present
study
aimed
to
investigate
the
effects
zein
peptides
on
C2C12
myoblasts
and
explore
their
potential
molecular
mechanisms.
proliferative,
cell
cycle,
anti-apoptotic
activities
were
evaluated.
Peptidomics
analysis
transcriptome
sequencing
employed
structure-activity
relationship
underlying
results
indicated
that
(0.05–0.2
mg/mL)
exerted
significant
proliferation-promoting
impact
cells,
via
increasing
viability
by
33.37
42.39%.
significantly
increased
S
phase
proportion
decreased
apoptosis
rate
from
34.08%
(model
group)
28.96%
cells.
In
addition,
exhibited
pronounced
effect
Zein
are
abundant
branch-chain
amino
acids,
especially
leucine.
Transcriptomics
revealed
can
promote
proliferation,
accelerate
improve
synthesis
muscle
cells
through
mTORC1
mTORC2
signaling
pathways.
Science Translational Medicine,
Journal Year:
2024,
Volume and Issue:
16(774)
Published: Nov. 20, 2024
Inflammatory
bowel
diseases
(IBDs)
are
chronic
debilitating
conditions
without
cure,
the
etiologies
of
which
unknown,
that
shorten
lifespans
7
million
patients
worldwide
by
nearly
10%.
Here,
we
found
decreased
autonomic
parasympathetic
tone
resulted
in
increased
IBD
susceptibility
and
mortality
mouse
models
disease.
Conversely,
vagal
stimulation
restored
neuromodulation
ameliorated
colitis
inhibiting
posttranslational
modification
SUMOylation
through
a
mechanism
independent
canonical
interleukin-10/α7
nicotinic
cholinergic
pathway.
Colonic
biopsies
from
with
IBDs
showed
an
increase
small
ubiquitin-like
modifier
(SUMO)2
SUMO3
during
active
In
global
genetic
knockout
models,
deletion
Sumo3
protected
against
development
delayed
onset
disease,
whereas
Sumo1
halted
progression
colitis.
Bone
marrow
transplants
-knockout
(KO)
but
not
-KO
mice
into
wild-type
conferred
protection
Electric
cervical
vagus
nerve
before
induction
inhibited
milder
symptoms
mice.
Treatment
TAK-981,
first-in-class
inhibitor
SUMO-activating
enzyme,
disease
three
murine
reduced
intestinal
permeability
bacterial
translocation
severe
model
suggesting
potential
to
reduce
sepsis.
These
results
reveal
pathway
reprograms
endogenous
stress-adaptive
responses
inhibition
suggest
as
therapeutic
target
for
IBD.
Biomedical Reports,
Journal Year:
2024,
Volume and Issue:
22(2)
Published: Nov. 25, 2024
Sepsis‑induced
myopathy
(SIM)
is
a
muscle
disease
caused
by
multiple
pathological
and
physiological
mechanisms
associated
with
sepsis.
The
pathogenesis
of
SIM
extremely
complex
still
unclear,
making
treatment
challenging.
At
present,
clinical
includes
early
functional
exercise,
respiratory
strength
training,
regulation
nutritional
structure
electrical
stimulation.
Drugs
targeting
the
ubiquitin‑proteasome
system,
autophagy‑lysosome
calpain
caspase
activation
pathways,
have
provided
potential
therapeutic
targets
for
atrophy.
Stem
cell
transplantation
therapy
brings
new
hope
SIM.
