Scope
Cachexia,
which
is
often
marked
by
skeletal
muscular
atrophy,
one
of
the
leading
causes
death
in
cancer
patients.
Astaxanthin,
a
carotenoid
obtained
from
marine
organisms
that
can
aid
prevention
and
treatment
variety
disorders.
In
this
study,
to
assess
whether
astaxanthin
ameliorates
weight
loss
muscle
atrophy
sorafenib‐treated
hepatocellular
carcinoma
mice
aimed.
Methods
results
H22
are
treated
with
30
mg
kg
−1
day
sorafenib
60
gavage
lasted
for
18
days.
Sorafenib
does
not
delay
loss,
although
it
reduce
tumor
burden.
Astaxanthin
dramatically
delays
sorafenib‐treating
mice,
without
affecting
food
intake.
inhibits
glycolysis,
slows
down
gluconeogenesis,
improves
insulin
resistance
tumor‐bearing
mice.
increases
glucose
competition
targeting
PI3K/Akt/GLUT4
signaling
pathway,
enhances
utilization
efficiency
muscle,
thereby
slowing
atrophy.
Conclusion
The
findings
show
significant
potential
as
nutritional
supplements
patients,
well
notion
interventions
should
be
implemented
at
initiation
treatment,
instead
waiting
until
cachexia
sets
in.
Frontiers in Cell and Developmental Biology,
Journal Year:
2021,
Volume and Issue:
9
Published: Sept. 14, 2021
Breast
cancer
represents
the
most
commonly
diagnosed
while
neoadjuvant
and
adjuvant
chemotherapies
are
extensively
used
in
order
to
reduce
tumor
development
improve
disease-free
survival.
However,
chemotherapy
also
leads
severe
off-target
side-effects
resulting,
together
with
itself,
major
skeletal
muscle
deconditioning.
This
review
first
focuses
on
recent
advances
both
macroscopic
changes
cellular
mechanisms
implicated
deconditioning
of
breast
patients,
particularly
as
a
consequence
treatment.
To
date,
only
six
clinical
studies
biopsies
patients
highlighted
several
important
aspects
such
decrease
fibers
cross-sectional
area,
dysregulation
protein
turnover
balance
mitochondrial
alterations.
comparison
knowledge
accumulated
through
decades
intensive
research
many
different
animal
human
models
atrophy,
more
necessary
obtain
comprehensive
understanding
processes
cancer-mediated
is
indeed
essential
ultimately
lead
implementation
efficient
preventive
strategies
exercise,
nutrition
or
pharmacological
treatments.
We
therefore
discuss
potential
by
drawing
parallel
other
cachexia
wasting,
at
pre-clinical
levels.
Cancers,
Journal Year:
2022,
Volume and Issue:
14(22), P. 5691 - 5691
Published: Nov. 19, 2022
Rapid
tumor
growth
requires
elevated
biosynthetic
activity,
supported
by
metabolic
rewiring
occurring
both
intrinsically
in
cancer
cells
and
extrinsically
the
host.
The
Warburg
effect
is
one
such
example,
burning
glucose
to
produce
a
continuous
flux
of
biomass
substrates
at
cost
energy
wasting
cycles
host
maintain
stable
glycemia.
Amino
acid
(AA)
metabolism
profoundly
altered
cells,
which
use
AAs
for
production
supporting
cell
proliferation.
peculiarities
AA
allow
identification
specific
vulnerabilities
as
targets
anti-cancer
treatments.
In
current
review,
approaches
targeting
terms
either
deprivation
or
supplementation
are
discussed.
Although
based
on
opposed
strategies,
show,
vitro
vivo,
positive
effects.
Any
AA-targeted
intervention
will
inevitably
impact
host,
who
frequently
already
has
cachexia.
Cancer
cachexia
syndrome,
also
due
malnutrition,
that
compromises
effectiveness
drugs
eventually
causes
patient’s
death.
may
exacerbate
malnutrition
cachexia,
while
improve
nutritional
status,
counteract
predispose
patient
more
effective
treatment.
Here
provided
an
attempt
describe
AA-based
therapeutic
integrate
currently
distant
points
view
cancer-centered
host-centered
research,
providing
glimpse
several
potential
investigations
approach
unique
disease.
Cancers,
Journal Year:
2024,
Volume and Issue:
16(10), P. 1921 - 1921
Published: May 18, 2024
Cancer
cachexia
is
a
multifaceted
syndrome
that
impacts
individuals
with
advanced
cancer.
It
causes
numerous
pathological
changes
in
cancer
patients,
such
as
inflammation
and
metabolic
dysfunction,
which
further
diminish
their
quality
of
life.
Unfortunately,
also
increases
the
risk
mortality
affected
individuals,
making
it
an
important
area
focus
for
research
treatment.
Several
potential
nutritional
therapies
are
being
tested
preclinical
clinical
models
efficacy
improving
muscle
metabolism
patients.
Despite
promising
results,
no
special
have
yet
been
validated
practice.
Multiple
studies
provide
evidence
benefits
increasing
protein
synthesis
through
increased
intake
amino
acids
or
protein.
There
exercise
can
reduce
atrophy
by
modulating
synthesis.
Therefore,
combination
may
be
more
effective
cachexia.
This
review
provides
overview
approaches
use
without
therapy
to
improve
Cancer Research,
Journal Year:
2020,
Volume and Issue:
80(9), P. 1861 - 1874
Published: March 4, 2020
Skeletal
muscle
wasting
is
a
devastating
consequence
of
cancer
that
contributes
to
increased
complications
and
poor
survival,
but
not
well
understood
at
the
molecular
level.
Herein,
we
investigated
role
Myocilin
(Myoc),
skeletal
hypertrophy-promoting
protein
showed
downregulated
in
multiple
mouse
models
cachexia.
Loss
Myoc
alone
was
sufficient
induce
phenotypes
identified
cachexia,
including
fiber
atrophy,
sarcolemmal
fragility,
impaired
regeneration.
By
18
months
age,
mice
deficient
significant
remodeling,
characterized
by
fat
collagen
deposition
compared
with
wild-type
mice,
thus
also
supporting
as
regulator
quality.
In
cachexia
models,
maintaining
expression
significantly
attenuated
loss,
while
lacking
enhanced
wasting.
Furthermore,
myocyte
enhancer
factor
2
C
(MEF2C)
transcription
key
upstream
activator
whose
gain
function
deterred
cancer-induced
dysfunction
preclinical
model
pancreatic
ductal
adenocarcinoma
(PDAC).
Finally,
noncancer
control
patients,
MYOC
reduced
patients
PDAC
defined
cachectic
correlated
MEF2c.
These
data
therefore
identify
disruptions
MEF2c-dependent
novel
mechanism
cancer-associated
similarly
disrupted
cancer.
SIGNIFICANCE:
This
work
identifies
transcriptional
mediates
murine
exhibiting
Experimental Biology and Medicine,
Journal Year:
2021,
Volume and Issue:
246(19), P. 2118 - 2127
Published: April 25, 2021
Cancer-induced
muscle
wasting,
i.e.
cachexia,
is
associated
with
different
types
of
cancer
such
as
pancreatic,
colorectal,
lung,
liver,
gastric
and
esophageal.
Cachexia
affects
prognosis
survival
in
cancer,
it
estimated
that
will
be
the
ultimate
cause
death
for
up
to
30%
patients.
Musculoskeletal
alterations
are
known
hallmarks
skeletal
atrophy
weakness
most
studied.
Recent
evidence
has
shed
light
on
presence
bone
loss
cachectic
patients,
even
absence
bone-metastatic
disease.
In
particular,
we
others
have
shown
communicate
by
exchanging
paracrine
endocrine
factors,
myokines
osteokines.
This
review
focus
describing
role
studied
myokines,
myostatin,
irisin,
metabolite
β-aminoisobutyric
acid,
BAIBA,
IL-6,
osteokines,
including
TGF-β,
osteocalcin,
sclerostin,
RANKL,
PTHrP,
FGF23,
lipid
mediator,
PGE2
during
cancer-induced
cachexia.
The
interplay
together
tumor-derived
soluble
characterizes
a
complex
clinical
scenario
which
musculoskeletal
amongst
debilitating
features.
Understanding
targeting
"secretome"
patients
likely
represent
promising
strategy
preserve
cachexia
thereby
enhancing
recovery.
Cells,
Journal Year:
2022,
Volume and Issue:
11(19), P. 3102 - 3102
Published: Oct. 1, 2022
Cancer
cachexia
is
a
muscle-wasting
syndrome
that
leads
to
severely
compromised
quality
of
life
and
increased
mortality.
A
strong
association
between
poor
prognosis
has
been
demonstrated
in
intractable
cancers,
including
glioblastoma
(GBM).
In
the
present
study,
it
was
ionizing
radiation
(IR),
first-line
treatment
for
GBM,
causes
cancer
by
increasing
exosomal
release
plasminogen
activator
inhibitor-1
(PAI-1)
from
cells.
Exosomal
PAI-1
delivered
skeletal
muscle
directly
penetrated
muscles
phosphorylates
STAT3
intensify
atrophy
activating
RING-finger
protein-1
(MuRF1)
F-box
(Atrogin1);
furthermore,
hampers
protein
synthesis
inhibiting
mTOR
signaling.
Additionally,
pharmacological
inhibition
TM5441
inhibited
rescued
synthesis,
thereby
providing
survival
benefits
GBM
orthotopic
xenograft
mouse
model.
summary,
our
data
delineated
role
induction
associated
with
radiotherapy-treated
GBM.
Our
also
indicated
targeting
could
serve
as
an
attractive
strategy
management
following
radiotherapy,
which
would
lead
considerable
improvement
patients
undergoing
radiotherapy.
Journal of Medicinal Food,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 20, 2025
Cancer
cachexia,
defined
by
the
gradual
depletion
of
muscle
and
fat
mass,
is
a
complex
multifactorial
syndrome
affecting
up
to
80%
cancer
patients.
This
study
investigated
effects
Curcuma
xanthorrhiza
extract
(CXE)
xanthorrhizol
(XAN)
in
ameliorating
cancer-induced
atrophy
BALB/c
mice.
Treatment
with
CXE
XAN
reversed
mass
loss,
grip
strength
decline,
decrease
myofiber
size
induced
cancer.
In
gastrocnemius
tissue,
downregulated
expression
nuclear
factor
kappa-beta
(NF-κB),
reducing
levels
proinflammatory
cytokines.
They
also
suppressed
catabolic
factors,
including
myostatin
ubiquitin-proteasome
E3
ligases,
translocation
forkhead
box
O3a.
Furthermore,
promoted
skeletal
anabolism
stimulating
myogenesis
activating
phosphoinositide
3-kinase/protein
kinase
B
signaling
pathway.
activation
subsequently
upregulated
mammalian
target
rapamycin
its
downstream
molecules.
Overall,
effectively
mitigated
catabolism
cachexia
may
serve
as
an
intervention
for
inhibiting
affected
patients
if
efficacy
can
be
confirmed
human
trials.
Al-Rafidain Journal of Medical Sciences ( ISSN 2789-3219 ),
Journal Year:
2025,
Volume and Issue:
8(2), P. 1 - 10
Published: April 3, 2025
Cancer
cachexia
affects
approximately
80%
of
cancer
patients
and
is
characterized
by
skeletal
muscle
wasting
reduced
fat
mass,
resulting
in
weight
loss
short
survival
time.
An
in-depth
understanding
the
mechanisms
can
provide
platforms
for
drug
non-pharmacological
management
this
condition
that
claims
life
around
20%
patients.
Most
current
work
field
pre-clinical
stages.
However,
such
preliminary
knowledge
anticipated
to
help
guide
design
large
comprehensive
clinical
trials
establish
safety
efficacy
therapeutic
interventions
treat
cachexia.
Current Opinion in Supportive and Palliative Care,
Journal Year:
2019,
Volume and Issue:
13(4), P. 279 - 285
Published: July 29, 2019
Overall
survival
of
patients
with
pancreatic
cancer
is
strongly
conditioned
by
tumor
biology
and
the
incidence
malnutrition
metabolic
disorders.
In
this
landscape,
assessment
body
composition
crucial
to
properly
manage
clinical
implications
muscle
wasting.
The
pathogenesis
condition
result
a
complex
interplay
between
host.
particular,
sarcopenia
induced
an
inadequate
nutritional
intake,
hormonal
abnormalities,
inflammation
imbalance
anabolic
catabolic
pathways.Recent
evidences
have
highlighted
role
in
patients,
revealing
prognostic
impact
on
morbidity,
mortality
survival.The
occurrence
could
amplify
chemotherapy-induced
toxicities,
prolong
hospitalizations
reduce
adherence
anticancer
treatment,
worsening
quality
life
survival.
Although
considerable
efforts
been
made
develop
treatment
strategies,
no
effective
interventions
identified
so
far.
Nevertheless,
if
promptly
adequately
supported,
might
benefit
from
adopted
dietary
intervention
avoid
further
loss
lean
mass.