Statins
are
among
the
most
widely
prescribed
drugs
for
treating
dyslipidemia
and
reducing
incidence
of
heart
disease
stroke.
However,
they
come
with
a
wide
range
side
effects,
from
myopathy
to
necrotizing
rhabdomyolysis,
as
well
diabetes,
hepatotoxicity,
sleep
problems.
The
common
effect
statins
is
statin-induced
myopathy,
often
leading
discontinuation
statin
therapy
noncompliance
in
many
patients.
This
study
aims
assess
effectiveness
coenzyme
Q10
(CoQ10)
supplementation
treatment
patients
myopathy.
systematic
review
was
conducted
by
following
Preferred
Reporting
Items
Systematic
Reviews
Meta-Analyses
(PRISMA)
2020
statement.
Relevant
studies
were
identified
through
searches
Medline,
PMC,
PubMed,
Science
Direct,
Google
Scholar.
Only
randomized
control
trials
meta-analyses
oral
CoQ10
versus
placebo
adults
statin-associated
myalgia
included.
risk
bias
assessed
using
Cochrane
Risk
Bias
tool
(The
Collaboration,
London,
England,
UK)
measurement
"assessment
multiple
reviews"
(AMSTAR
tool).
Out
5,000
records
identified,
only
five
selected
this
review:
one
meta-analysis
four
controlled
trials.
All
these
between
2010
2023,
involving
total
800
showed
improvement
supplementation,
along
or
without
reduced
dosage
statins,
any
notable
effects
CoQ10.
Therefore,
it
can
be
deduced
that
significantly
ameliorates
musculoskeletal
symptoms.
Cell Death Discovery,
Год журнала:
2024,
Номер
10(1)
Опубликована: Апрель 8, 2024
Abstract
Mitochondria
are
major
organelles
involved
in
several
processes
related
to
energy
supply,
metabolism,
and
cell
proliferation.
The
mitochondria
function
is
transcriptionally
regulated
by
DNA
(mtDNA),
which
encodes
the
key
proteins
electron
transport
chain
that
indispensable
for
oxidative
phosphorylation
(OXPHOS).
Mitochondrial
transcriptional
abnormalities
closely
a
variety
of
human
diseases,
such
as
cardiovascular
diabetes.
transcription
mtDNA,
mitochondrial
RNA
polymerase
(POLRMT),
two
factors
(TFAM
TF2BM),
one
elongation
(TEFM),
known
termination
factor
(mTERFs).
Dysregulation
these
directly
leads
altered
expression
mtDNA
tumor
cells,
resulting
cellular
metabolic
reprogramming
dysfunction.
This
dysregulation
plays
role
modulating
progression.
Therefore,
understanding
cancer
can
have
implications
diagnosis,
prognosis,
treatment.
Targeting
or
pathways
may
provide
potential
therapeutic
strategies
Additionally,
assessing
profiles
biomarkers
cells
patient
samples
offer
diagnostic
prognostic
information.
Cellular & Molecular Biology Letters,
Год журнала:
2024,
Номер
29(1)
Опубликована: Апрель 23, 2024
Abstract
Skeletal
muscle
is
the
largest
metabolic
organ
of
human
body.
Maintaining
best
quality
control
and
functional
integrity
mitochondria
essential
for
health
skeletal
muscle.
However,
mitochondrial
dysfunction
characterized
by
dynamic
imbalance
mitophagy
disruption
can
lead
to
varying
degrees
atrophy,
but
underlying
mechanism
action
still
unclear.
Although
dynamics
are
two
different
mechanisms,
a
large
amount
evidence
has
indicated
that
they
interrelated
mutually
regulated.
The
former
maintains
balance
network,
eliminates
damaged
or
aged
mitochondria,
enables
cells
survive
normally.
latter
degrades
through
lysosomal
pathway,
ensuring
cellular
homeostasis.
atrophy
considered
an
urgent
global
issue.
Understanding
gaining
knowledge
about
caused
dysfunction,
particularly
focusing
on
autophagy,
greatly
contribute
prevention
treatment
atrophy.
In
this
review,
we
critically
summarize
recent
research
progress
in
expound
intrinsic
molecular
mitophagy.
Importantly,
emphasize
potential
targeting
as
therapeutic
strategies
including
pharmacological
exercise
therapy,
effective
methods
Neurological Sciences,
Год журнала:
2024,
Номер
45(9), С. 4121 - 4131
Опубликована: Апрель 27, 2024
Amyotrophic
lateral
sclerosis
(ALS)
is
a
progressive
and
fatal
neuromuscular
disease
that
results
in
the
loss
of
motor
neurons
severe
skeletal
muscle
atrophy.
The
etiology
ALS
linked
to
muscle,
which
can
activate
retrograde
signaling
cascade
destroys
neurons.
This
why
satellite
cells
mitochondria
play
crucial
role
health
performance
muscles.
review
presents
current
knowledge
on
involvement
mitochondrial
dysfunction,
atrophy,
cells,
junction
(NMJ)
ALS.
It
also
discusses
therapeutic
strategies,
including
exercise,
drugs,
stem
gene
therapy,
prospective
use
transplantation
as
viable
strategy.
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 19, 2025
Abstract
Sarcopenia,
or
age-related
muscle
dysfunction,
contributes
to
morbidity
and
mortality.
Besides
decreases
in
force,
sarcopenia
is
associated
with
atrophy
fast-to-slow
fiber
type
switching,
which
typically
secondary
denervation
humans
rodents.
However,
very
little
known
about
cellular
changes
preceding
these
important
(mal)adaptations.
To
this
matter,
mitochondria
the
sarcoplasmic
reticulum
are
critical
for
tension
generation
myofibers.
They
physically
interact
at
boundaries
of
sarcomeres
forming
subcellular
hubs
called
mitochondria-endo/sarcoplasmic
contacts
(MERCs).
Yet,
whether
MERCs
ultrastructure
proteome
occur
early
aging
unknown.
Here,
studying
young
adult
older
mice
we
reveal
that
slows
relaxation
leading
longer
excitation-contraction-relaxation
(ECR)
cycles
before
maximal
force
switching
takes
place.
We
MERC
mitochondria-associated
ER
membrane
(MAM)
protein
composition
also
affected
closely
rate
relaxation.
Additionally,
demonstrate
regular
exercise
preserves
aging.
Finally,
profile
a
set
MAM
proteins
involved
energy
metabolism,
quality
control,
Ca
2+
homeostasis,
cytoskeleton
integrity
redox
balance
inversely
regulated
by
exercise.
These
may
represent
new
targets
preserve
function
individuals.
Frontiers in Molecular Biosciences,
Год журнала:
2025,
Номер
12
Опубликована: Март 19, 2025
In
skeletal
muscle,
calcium
is
not
only
essential
to
stimulate
and
sustain
their
contractions
but
also
for
muscle
embryogenesis,
regeneration,
energy
production
in
mitochondria,
fusion.
Different
ion
channels
contribute
achieving
the
various
functions
of
muscles.
Muscle
contraction
initiated
by
releasing
from
sarcoplasmic
reticulum
through
ryanodine
receptor
gated
mechanically
four
dihydropyridine
receptors
T-tubules.
The
influx
store-operated
sustains
stimulates
regeneration.
Mitochondrial
uniporter
allows
entry
into
mitochondria
oxidative
phosphorylation.
Aging
alters
expression
activity
these
different
channels,
resulting
a
reduction
force
generation
regeneration
capacity.
Regular
physical
training
bioactive
molecules
nutrients
can
prevent
effects
aging
on
channels.
This
review
focuses
current
knowledge
muscles’
Nutrients,
Год журнала:
2025,
Номер
17(7), С. 1217 - 1217
Опубликована: Март 30, 2025
Background/Objectives:
Muscle
atrophy,
defined
by
diminished
muscle
mass
and
function,
is
a
notable
concern
associated
with
aging,
disease,
glucocorticoid
treatment.
Pueraria
montana
var.
lobata
extract
(PMLE)
demonstrates
multiple
bioactive
properties,
such
as
antioxidant,
anti-inflammatory,
metabolic
regulatory
activities;
however,
its
role
in
atrophy
has
not
been
extensively
investigated
to
date.
This
study
examined
how
PMLE
influences
both
cell
differentiation
dexamethasone
(DEX)-induced
degeneration
focusing
on
the
underlying
molecular
mechanisms.
Methods:
effects
of
myogenic
DEX-induced
atrophy.
C2C12
myoblasts
were
treated
(10-100
ng/mL)
assessed
for
changes
expression
myogenesis-related
genes
activation
Akt/mTOR
AMPK/SIRT1/PGC-1α
signaling
cascades.
In
vivo,
model
was
used
assess
mass,
fiber
morphology,
changes.
Results:
promoted
development
increasing
MyHC,
MyoD,
myogenin
while
activating
protein
synthesis
mitochondrial
biogenesis
pathways.
counteracted
myotube
restoring
diameter
promoting
cellular
fusion
vitro.
mitigated
degradation
fast-twitch
groups
reversed
suppression
key
anabolic
Conclusions:
These
findings
suggest
that
promotes
protects
against
regulating
critical
pathways,
indicating
promise
treatment
candidate
conditions
involving
wasting.
Further
studies
are
required
clinical
application
long-term
safety
efficacy.
Aging and Disease,
Год журнала:
2024,
Номер
unknown
Опубликована: Янв. 1, 2024
Aging
is
an
inevitable
and
complex
biological
process
involving
multi-factorial
mechanisms.
Mitochondrial
dysfunction
a
critical
factor
in
the
aging
process,
characterized
by
decline
mitochondrial
quality
activity,
leading
to
aging-related
diseases.
Therefore,
mitochondria
have
become
attractive
target
anti-aging
therapies.
Several
senolytic
drugs
targeting
antioxidant
agents
been
used
research
past
few
years.
However,
these
strategies
may
cause
adverse
effects
with
long-term
medication.
In
this
extensive
review,
we
propose
"mitochondrial
transplantation,"
which
transfers
healthy
from
donor
cells
recipient
replace
damaged
or
dysfunctional
mitochondria,
as
new
alternative
strategy
for
treating
aging-associated
introduce
contemporary
landscape
of
transplantation,
then
discuss
intensely
successful
applications
transplantation
therapy
diseases
such
neurodegenerative
diseases,
cardiovascular
aging,
reproductive
highlighting
its
translational
potential.
Finally,
summarize
prospect
challenges
opportunities
faces
therapy.
