Journal of Translational Medicine,
Journal Year:
2023,
Volume and Issue:
21(1)
Published: July 26, 2023
Abstract
Mitochondria
play
important
roles
in
maintaining
cellular
homeostasis
and
skeletal
muscle
health,
damage
to
mitochondria
can
lead
a
series
of
pathophysiological
changes.
Mitochondrial
dysfunction
atrophy,
its
molecular
mechanism
leading
atrophy
is
complex.
Understanding
the
pathogenesis
mitochondrial
useful
for
prevention
treatment
finding
drugs
methods
target
modulate
function
are
urgent
tasks
atrophy.
In
this
review,
we
first
discussed
normal
muscle.
Importantly,
described
effect
on
mechanisms
involved.
Furthermore,
regulatory
different
signaling
pathways
(AMPK-SIRT1-PGC-1α,
IGF-1-PI3K-Akt-mTOR,
FoxOs,
JAK-STAT3,
TGF-β-Smad2/3
NF-κB
pathways,
etc.)
factors
were
investigated
dysfunction.
Next,
analyzed
manifestations
caused
by
diseases.
Finally,
summarized
preventive
therapeutic
effects
targeted
regulation
including
drug
therapy,
exercise
diet,
gene
stem
cell
therapy
physical
therapy.
This
review
great
significance
holistic
understanding
role
muscle,
which
helpful
researchers
further
has
an
inspiring
development
strategies
targeting
future.
Molecular Biomedicine,
Journal Year:
2023,
Volume and Issue:
4(1)
Published: Nov. 8, 2023
Abstract
The
Janus
kinase-signal
transducer
and
transcription
activator
pathway
(JAK-STAT)
serves
as
a
cornerstone
in
cellular
signaling,
regulating
physiological
pathological
processes
such
inflammation
stress.
Dysregulation
this
can
lead
to
severe
immunodeficiencies
malignancies,
its
role
extends
neurotransduction
pro-inflammatory
signaling
mechanisms.
Although
JAK
inhibitors
(Jakinibs)
have
successfully
treated
immunological
inflammatory
disorders,
their
application
has
generally
been
limited
diseases
with
similar
pathogenic
features.
Despite
the
modest
expression
of
JAK-STAT
CNS,
it
is
crucial
for
functions
cortex,
hippocampus,
cerebellum,
making
relevant
conditions
like
Parkinson's
disease
other
neuroinflammatory
disorders.
Furthermore,
influence
on
serotonin
receptors
phospholipase
C
implications
stress
mood
This
review
expands
understanding
JAK-STAT,
moving
beyond
traditional
contexts
explore
stress-related
disorders
CNS
function.
Recent
findings,
effectiveness
Jakinibs
chronic
rheumatoid
arthritis,
expand
therapeutic
applicability.
Advances
isoform-specific
inhibitors,
including
filgotinib
upadacitinib,
promise
greater
specificity
fewer
off-target
effects.
Combination
therapies,
involving
monoclonal
antibodies,
aiming
enhance
efficacy
also
give
great
hope.
Overall,
bridges
gap
between
basic
science
clinical
application,
elucidating
complex
human
health
guiding
future
interventions.
Graphical
Cell Communication and Signaling,
Journal Year:
2025,
Volume and Issue:
23(1)
Published: Jan. 9, 2025
This
review
comprehensively
explores
the
critical
role
of
calcium
as
an
essential
small-molecule
biomessenger
in
skeletal
muscle
function.
Calcium
is
vital
for
both
regulating
excitation–contraction
coupling
and
development,
maintenance,
regeneration
cells.
The
orchestrated
release
from
endoplasmic
reticulum
(ER)
mediated
by
receptors
such
ryanodine
receptor
(RYR)
inositol
1,4,5-trisphosphate
(IP3R),
which
crucial
contraction.
sarcoendoplasmic
ATPase
(SERCA)
pump
plays
a
key
recapturing
calcium,
enabling
to
return
relaxed
state.
A
pivotal
aspect
homeostasis
involves
dynamic
interaction
between
mitochondria
ER.
includes
local
signaling
facilitated
RYRs
"quasi-synaptic"
mechanism
formed
IP3R-Grp75-VDAC/MCU
axis,
allowing
rapid
uptake
with
minimal
interference
at
cytoplasmic
level.
Disruption
transport
can
lead
mitochondrial
overload,
triggering
opening
permeability
transition
pore
subsequent
reactive
oxygen
species
cytochrome
C,
ultimately
resulting
damage
atrophy.
complex
relationship
ER
how
these
organelles
regulate
levels
muscle,
aiming
provide
valuable
perspectives
future
research
on
pathogenesis
diseases
development
prevention
strategies.
Nutrients,
Journal Year:
2023,
Volume and Issue:
15(24), P. 5127 - 5127
Published: Dec. 16, 2023
Aging
is
characterized
by
significant
physiological
changes,
with
the
degree
of
decline
varying
significantly
among
individuals.
The
preservation
intrinsic
capacity
over
course
an
individual's
lifespan
fundamental
for
healthy
aging.
Locomotion,
which
entails
independent
movement,
intricately
connected
various
dimensions
human
life,
including
cognition,
vitality,
sensory
perception,
and
psychological
well-being.
Notably,
skeletal
muscle
functions
as
a
pivotal
nexus
within
this
intricate
framework.
Any
perturbation
in
its
functionality
can
manifest
compromised
physical
performance
elevated
susceptibility
to
frailty.
Magnesium
essential
mineral
that
plays
central
role
approximately
800
biochemical
reactions
body.
Its
distinctive
chemical
attributes
render
it
indispensable
stabilizing
factor
orchestration
diverse
cellular
organelle
functions,
thereby
rendering
irreplaceable
processes
directly
impacting
health.
This
narrative
review
offers
comprehensive
exploration
played
magnesium
maintaining
integrity,
emphasizing
critical
importance
optimal
levels
promoting
Critical Care,
Journal Year:
2024,
Volume and Issue:
28(1)
Published: Feb. 1, 2024
Abstract
The
optimal
feeding
strategy
for
critically
ill
patients
is
still
debated,
but
must
be
adapted
to
individual
patient
needs.
Critically
are
at
risk
of
muscle
catabolism,
leading
loss
mass
and
its
consequent
clinical
impacts.
Timing
introduction
protein
targets
have
been
explored
in
recent
trials.
These
suggest
that
“moderate”
provision
(maximum
1.2
g/kg/day)
best
during
the
initial
stages
illness.
Unresolved
inflammation
may
a
key
factor
driving
catabolism.
omega-3
(n-3)
fatty
acids
eicosapentaenoic
acid
(EPA)
docosahexaenoic
(DHA)
substrates
synthesis
mediators
termed
specialized
pro-resolving
or
SPMs
actively
resolve
inflammation.
There
evidence
from
other
settings
high-dose
oral
EPA
+
DHA
increases
synthesis,
decreases
breakdown,
maintains
mass.
responsible
some
these
effects,
especially
upon
breakdown.
Given
findings,
as
part
medical
nutritional
therapy
seems
prevent
persistence
related
anabolic
resistance
loss.
Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
15
Published: Jan. 19, 2024
Aim:
Diabetic
sarcopenia
leads
to
disability
and
seriously
affects
the
quality
of
life.
Currently,
there
are
no
effective
therapeutic
strategies
for
diabetic
sarcopenia.
Our
previous
studies
have
shown
that
inflammation
plays
a
critical
role
in
skeletal
muscle
atrophy.
Interestingly,
connection
between
chronic
complications
has
been
revealed.
However,
effects
non-steroidal
anti-inflammatory
drug
celecoxib
on
remains
unclear.
Materials
Methods:
The
streptozotocin
(streptozotocin)-induced
model
was
established.
Rotarod
test
grip
strength
were
used
assess
function.
Hematoxylin
eosin
immunofluorescence
staining
performed
evaluate
inflammatory
infiltration
morphology
motor
endplates
muscles.
Succinate
dehydrogenase
(SDH)
determine
number
succinate
dehydrogenase-positive
fibers.
Dihydroethidium
levels
reactive
oxygen
species
(ROS).
Western
blot
measure
proteins
involved
inflammation,
oxidative
stress,
endoplasmic
reticulum
ubiquitination,
autophagic-lysosomal
pathway.
Transmission
electron
microscopy
mitophagy.
Results:
Celecoxib
significantly
ameliorated
atrophy,
improving
function
preserving
mice.
also
decreased
cell,
reduced
IL-6
TNF-α,
suppressed
activation
NF-κB,
Stat3,
NLRP3
inflammasome
pathways
levels,
downregulated
Nox2
Nox4,
upregulated
GPX1
Nrf2,
further
stress
by
inhibiting
Perk-EIF-2α-ATF4-Chop
inhibited
Foxo3a,
Fbx32
MuRF1
ubiquitin-proteasome
system,
as
well
BNIP3,
Beclin1,
ATG7,
LC3Ⅱ
protected
mitochondria
promoted
mitochondrial
biogenesis
elevating
SIRT1
PGC1-α,
increased
SDH-positive
fibers
Conclusion:
improved
protecting
mitochondria,
subsequently
suppressing
proteolytic
systems.
study
provides
evidences
molecular
mechanism
treatment
sarcopenia,
broaden
way
new
use
