Molecular Metabolism,
Год журнала:
2022,
Номер
67, С. 101652 - 101652
Опубликована: Дек. 9, 2022
Recent
work
has
established
associations
between
elevated
p21,
the
accumulation
of
senescent
cells,
and
skeletal
muscle
dysfunction
in
mice
humans.
Using
a
mouse
model
p21
overexpression
(p21OE),
we
examined
if
mechanistically
contributes
to
cellular
senescence
pathological
features
muscle.
We
show
that
induces
several
core
properties
muscle,
including
an
altered
transcriptome,
DNA
damage,
mitochondrial
dysfunction,
senescence-associated
secretory
phenotype
(SASP).
Furthermore,
p21OE
exhibit
manifestations
pathology,
such
as
atrophy,
fibrosis,
impaired
physical
function
when
compared
age-matched
controls.
These
findings
suggest
alone
is
sufficient
drive
program
reveal
novel
source
loss
dysfunction.
Inflammation and Regeneration,
Год журнала:
2024,
Номер
44(1)
Опубликована: Июнь 3, 2024
Abstract
Cellular
senescence
is
the
state
in
which
cells
undergo
irreversible
cell
cycle
arrest
and
acquire
diverse
phenotypes.
It
has
been
linked
to
chronic
inflammation
fibrosis
various
organs
as
well
individual
aging.
Therefore,
eliminating
senescent
emerged
a
potential
target
for
extending
healthy
lifespans.
plays
beneficial
role
many
biological
processes,
including
embryonic
development,
wound
healing,
tissue
regeneration,
mediated
by
activation
of
stem
cells.
comprehensive
understanding
cellular
senescence,
both
its
detrimental
effects,
critical
developing
safe
effective
treatment
strategies
This
review
provides
an
overview
pathological
roles
with
particular
focus
on
or
functions
among
roles.
Clinical and Experimental Medicine,
Год журнала:
2025,
Номер
25(1)
Опубликована: Янв. 23, 2025
Cellular
senescence
is
understood
to
be
a
biological
process
that
defined
as
irreversible
growth
arrest
and
was
originally
recognized
tumor-suppressive
mechanism
prevents
further
propagation
of
damaged
cells.
More
recently,
cellular
has
been
shown
have
dual
role
in
prevention
tumor
promotion.
Senescent
cells
carry
senescence-associated
secretory
phenotype
(SASP),
which
altered
by
factors
including
pro-inflammatory
cytokines,
chemokines,
other
proteases,
leading
the
alteration
tissue
microenvironment.
Though
would
eventually
halt
cancerous
potential
cells,
SASP
contributes
environment
promoting
inflammation,
matrix
remodeling,
cell
invasion.
The
paradox
prevention/promotion
particularly
relevant
bone
niche
microenvironment,
where
longer-lasting,
chronic
inflammation
promotes
formation.
Insights
into
mechanistic
understanding
provide
basis
for
targeted
therapies,
such
senolytics,
aim
eliminate
senescent
or
inhibitors,
tumor-promoting
effects
senescence.
These
therapeutic
interventions
offer
significant
clinical
implications
treating
cancer
healthy
aging.
Molecular Metabolism,
Год журнала:
2022,
Номер
67, С. 101652 - 101652
Опубликована: Дек. 9, 2022
Recent
work
has
established
associations
between
elevated
p21,
the
accumulation
of
senescent
cells,
and
skeletal
muscle
dysfunction
in
mice
humans.
Using
a
mouse
model
p21
overexpression
(p21OE),
we
examined
if
mechanistically
contributes
to
cellular
senescence
pathological
features
muscle.
We
show
that
induces
several
core
properties
muscle,
including
an
altered
transcriptome,
DNA
damage,
mitochondrial
dysfunction,
senescence-associated
secretory
phenotype
(SASP).
Furthermore,
p21OE
exhibit
manifestations
pathology,
such
as
atrophy,
fibrosis,
impaired
physical
function
when
compared
age-matched
controls.
These
findings
suggest
alone
is
sufficient
drive
program
reveal
novel
source
loss
dysfunction.
