Abstract
Adult
skeletal
muscle
stem
cells
(MuSCs)
are
essential
for
homeostasis
and
regeneration.
During
aging,
the
number
of
MuSCs
their
regenerative
capacity
gradually
decline
but
underlying
mechanisms
remain
elusive.
Here,
we
identify
Sugt1
(suppressor
G2
allele
SKP1
homolog),
which
is
a
chaperone
kinetochore
function
during
mitosis
regeneration
by
regulating
MuSC
proliferation.
expression
level
low
in
quiescent
highly
induced
when
become
activated
expand
as
proliferating
myoblasts.
Inducible
inactivation
causes
impaired
upon
acute
injury
impairing
Furthermore,
loss
leads
to
cell
cycle
arrest
G2/M
phase
cellular
senescence.
Moreover,
long-term
results
precocious
aging
inhibiting
proliferation
promoting
Mechanistically,
cytosolic
E3
ubiquitin-ligase,
Trim21
protein
interacting
partner
myoblast
cells.
We
further
demonstrate
that
promotes
ubiquitination
p21
via
Trim21;
accumulation
inhibit
progression
stimulates
Collectively,
our
findings
uncover
an
regulator
aging.
Antioxidants,
Год журнала:
2023,
Номер
12(3), С. 651 - 651
Опубликована: Март 6, 2023
Aging
is
a
complex
biological
process
accompanied
by
progressive
decline
in
the
physical
function
of
organism
and
an
increased
risk
age-related
chronic
diseases
such
as
cardiovascular
diseases,
cancer,
neurodegenerative
diseases.
Studies
have
established
that
there
exist
nine
hallmarks
aging
process,
including
(i)
telomere
shortening,
(ii)
genomic
instability,
(iii)
epigenetic
modifications,
(iv)
mitochondrial
dysfunction,
(v)
loss
proteostasis,
(vi)
dysregulated
nutrient
sensing,
(vii)
stem
cell
exhaustion,
(viii)
cellular
senescence,
(ix)
altered
communication.
All
these
alterations
been
linked
to
sustained
systemic
inflammation,
mechanisms
contribute
timing
not
clearly
determined
yet.
Nevertheless,
dysfunction
one
most
important
contributing
process.
Mitochondria
primary
endogenous
source
reactive
oxygen
species
(ROS).
During
ATP
production
elevated
ROS
together
with
antioxidant
defense.
Elevated
levels
can
cause
oxidative
stress
severe
damage
cell,
organelle
membranes,
DNA,
lipids,
proteins.
This
contributes
phenotype.
In
this
review,
we
summarize
recent
advances
emphasis
on
production.
Cellular Signalling,
Год журнала:
2022,
Номер
96, С. 110355 - 110355
Опубликована: Май 17, 2022
Muscle
atrophy
and
sarcopenia
(the
term
given
to
the
age-related
decline
in
muscle
mass
function),
influence
an
individuals
risk
of
falls,
frailty,
functional
decline,
and,
ultimately,
impaired
quality
life.
Vitamin
D
deficiency
(low
serum
levels
25-hydroxyvitamin
(25(OH)D3))
has
been
reported
impair
strength
increase
sarcopenia.
The
mechanisms
that
underpin
link
between
low
25(OH)D3
are
yet
be
fully
understood
but
several
lines
evidence
have
highlighted
importance
both
genomic
non-genomic
effects
active
vitamin
(1,25-dihydroxyvitamin
(1,25(OH)2D3))
its
nuclear
receptor
(VDR),
skeletal
functioning.
Studies
vitro
demonstrated
a
key
role
for
D/VDR
axis
regulating
biological
processes
central
sarcopenic
atrophy,
such
as
proteolysis,
mitochondrial
function,
cellular
senescence,
adiposity.
aim
this
review
is
provide
mechanistic
overview
proposed
atrophy.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(8), С. 4300 - 4300
Опубликована: Апрель 12, 2024
Sarcopenia
is
a
prevalent
degenerative
skeletal
muscle
condition
in
the
elderly
population,
posing
tremendous
burden
on
diseased
individuals
and
healthcare
systems
worldwide.
Conventionally,
sarcopenia
currently
managed
through
nutritional
interventions,
physical
therapy,
lifestyle
modification,
with
no
pharmaceutical
agents
being
approved
for
specific
use
this
disease.
As
pathogenesis
of
still
poorly
understood
there
treatment
recognized
as
universally
effective,
recent
research
efforts
have
been
directed
at
better
comprehending
illness
diversifying
strategies.
In
respect,
paper
overviews
new
advances
correlation
its
underlying
mechanisms.
Specifically,
review
creates
an
updated
framework
sarcopenia,
describing
etiology,
pathogenesis,
risk
factors,
conventional
treatments,
further
discussing
emerging
therapeutic
approaches
like
drug
formulations,
delivery
systems,
stem
cell
therapies,
tissue-engineered
scaffolds
more
detail.
The
triad
of
vascular
impairment,
muscle
atrophy,
and
cognitive
decline
represents
critical
age-related
conditions
that
significantly
impact
health.
Vascular
impairment
disrupts
blood
flow,
precipitating
mass
reduction
seen
in
sarcopenia
the
neuronal
functions
characteristic
neurodegeneration.
Our
limited
understanding
intricate
relationships
within
this
hinders
accurate
diagnosis
effective
treatment
strategies.
This
review
ana-lyzes
interrelated
mechanisms
contribute
to
these
conditions,
with
a
specific
focus
on
ox-idative
stress,
chronic
inflammation,
impaired
nutrient
delivery.
aim
is
understand
common
pathways
involved
suggest
comprehensive
therapeutic
approaches.
dysfunctions
hinder
circulation
transportation
nutrients,
resulting
sar-copenia
characterized
by
atrophy
weakness.
dysfunction
have
negative
physical
function
quality
life.
Neurodegenerative
diseases
exhibit
comparable
pathophysiological
affect
motor
functions.
Preventive
approaches
encompass
lifestyle
adjustments,
addressing
oxidative
in-flammation,
integrated
therapies
improving
muscular
well-being.
Better
links
can
refine
strategies
yield
better
patient
out-comes.
study
emphasizes
complex
interplay
between
dysfunction,
de-generation,
decline,
highlighting
necessity
for
multidisciplinary
ap-proaches.
Advances
domain
promise
improved
diagnostic
accuracy,
more
thera-peutic
options,
enhanced
preventive
measures,
all
contributing
higher
life
elderly
population.
Frontiers in Molecular Biosciences,
Год журнала:
2024,
Номер
10
Опубликована: Янв. 9, 2024
Muscle
aging
is
a
complex
physiological
process
that
leads
to
the
progressive
decline
in
muscle
mass
and
function,
contributing
debilitating
conditions
elderly
such
as
sarcopenia.
In
recent
years,
non-coding
RNAs
(ncRNAs)
have
been
increasingly
recognized
major
regulators
of
related
cellular
processes.
Here,
we
comprehensively
review
emerging
role
ncRNAs,
including
microRNAs
(miRNAs),
long
(lncRNAs),
circular
(circRNAs),
regulation
aging.
We
also
discuss
how
targeting
these
ncRNAs
can
be
explored
for
development
novel
interventions
combat
age-related
decline.
The
insights
provided
this
offer
promising
avenue
future
research
therapeutic
strategies
aimed
at
improving
health
during
FEBS Journal,
Год журнала:
2022,
Номер
290(5), С. 1221 - 1234
Опубликована: Апрель 23, 2022
The
human
genome
is
capable
of
producing
hundreds
thousands
different
proteins
and
non-coding
RNAs
from
<20
000
genes,
in
a
co-ordinated
regulated
fashion.
This
achieved
by
collection
phenomena
known
as
mRNA
processing
metabolism,
encompasses
events
the
life
cycle
an
RNA
synthesis
to
degradation.
These
factors
are
critical
determinants
cellular
adaptability
plasticity,
which
allows
cell
adjust
its
transcriptomic
output
response
internal
external
environment.
Evidence
building
that
dysfunctional
metabolism
may
be
key
contributor
development
senescence.
Senescent
cells
definition
have
exited
cycle,
but
gained
functional
features
such
secretion
senescence-associated
secretory
phenotype
(SASP),
driver
chronic
disease
perhaps
even
ageing
itself.
In
this
review,
I
will
outline
impact
dysregulated
on
senescence
at
level
systems,
describe
mechanisms
progressive
deterioration
these
processes
organismal
ageing.
Finally,
present
evidence
implicating
important
process
new
hallmark
ageing,
could
harnessed
future
develop
senotherapeutic
interventions
for
disease.
