Frontiers in Aging,
Journal Year:
2022,
Volume and Issue:
3
Published: Feb. 4, 2022
The
risk
of
morbidity
and
mortality
increases
exponentially
with
age.
Chronic
inflammation,
accumulation
DNA
damage,
dysfunctional
mitochondria,
increased
senescent
cell
load
are
factors
contributing
to
this.
Mechanistic
investigations
have
revealed
specific
pathways
processes
which,
proposedly,
cause
age-related
phenotypes
such
as
frailty,
reduced
physical
resilience,
multi-morbidity.
Among
promising
treatments
alleviating
the
consequences
aging
caloric
restriction
pharmacologically
targeting
longevity
mechanistic
target
rapamycin
(mTOR),
sirtuins,
anti-apoptotic
in
cells.
Regulation
these
has
significant
health-
lifespan
extending
results
animal
models.
Nevertheless,
it
remains
unclear
if
similar
translate
humans.
A
requirement
translation
development
age-
associated
biomarkers
longitudinal
trials
difficult
not
feasible,
practical,
nor
ethical
when
human
life
span
is
endpoint.
Current
anti-aging
intervention
studies
humans
will
be
covered
within
this
paper.
future
clinical
may
phase
2
3
larger
populations
safety
tolerability
investigated
medication
continues
a
hurdle
for
further
investigations.
Cell & Bioscience,
Journal Year:
2022,
Volume and Issue:
12(1)
Published: May 31, 2022
Abstract
Background
The
global
population
of
older
individuals
is
growing,
and
ageing
a
key
risk
factor
for
atherosclerotic
cardiovascular
diseases.
Abnormal
accumulation
senescent
cells
can
cause
potentially
deleterious
effects
on
the
organism
with
age.
As
vital
marker
cellular
senescence,
senescence-associated
secretory
phenotype
(SASP)
novel
mechanism
to
link
senescence
atherosclerosis.
Main
body
In
this
review,
we
concretely
describe
characteristics
SASP
its
regulation
mechanisms.
Importantly,
provide
perspectives
how
promote
from
different
types
have
roles
in
atherosclerosis
progression.
significant
mediator
harmful
cells,
it
play
pro-atherogenic
role
by
producing
inflammation
immune
dysfunction.
Furthermore,
deliver
signals
surrounding
vascular
gradually
contributing
development
Finally,
focus
variety
therapeutic
strategies
aimed
reduce
burden
elderly
targeting
inhibiting
regulatory
mechanisms
SASP.
Conclusion
This
review
systematically
summarizes
multiple
contribute
exploration
new
opportunities.
Frontiers in Cell and Developmental Biology,
Journal Year:
2022,
Volume and Issue:
9
Published: Jan. 10, 2022
Aging
promotes
most
degenerative
pathologies
in
mammals,
which
are
characterized
by
progressive
decline
of
function
at
molecular,
cellular,
tissue,
and
organismal
levels
account
for
a
host
health
care
expenditures
both
developing
developed
nations.
Sarcopenia
is
prominent
age-related
disorder
musculoskeletal
system.
Defined
as
gradual
generalized
chronic
skeletal
muscle
disorder,
sarcopenia
involves
accelerated
loss
mass,
strength
function,
associated
with
increased
adverse
functional
outcomes
evolutionally
refers
to
wasting
accompanied
other
geriatric
syndromes.
More
efforts
have
been
made
clarify
mechanisms
underlying
new
findings
suggest
that
it
may
be
feasible
delay
modulating
fundamental
such
cellular
senescence.
Cellular
senescence
the
essentially
irreversible
growth
arrest
mainly
regulated
p53/p21
CIP1
p16
INK4a
/pRB
pathways
organism
ages,
possibly
detrimentally
contributing
via
stem
cells
(MuSCs)
dysfunction
senescence-associated
secretory
phenotype
(SASP)
while
beneficial
functions
counteracting
cancer
progression,
tissue
regeneration
wound
healing.
By
now
diverse
studies
mice
humans
established
targeting
powerful
strategy
alleviating
sarcopenia.
However,
through
senescent
contribute
progression
need
further
researched.
We
review
possible
involved
SASP
resulting
from
senescence,
their
associations
sarcopenia,
current
emerging
therapeutic
opportunities
based
on
relevant
potential
paths
clinical
interventions
genetically
or
pharmacologically.
Frontiers in Aging,
Journal Year:
2022,
Volume and Issue:
3
Published: Feb. 4, 2022
The
risk
of
morbidity
and
mortality
increases
exponentially
with
age.
Chronic
inflammation,
accumulation
DNA
damage,
dysfunctional
mitochondria,
increased
senescent
cell
load
are
factors
contributing
to
this.
Mechanistic
investigations
have
revealed
specific
pathways
processes
which,
proposedly,
cause
age-related
phenotypes
such
as
frailty,
reduced
physical
resilience,
multi-morbidity.
Among
promising
treatments
alleviating
the
consequences
aging
caloric
restriction
pharmacologically
targeting
longevity
mechanistic
target
rapamycin
(mTOR),
sirtuins,
anti-apoptotic
in
cells.
Regulation
these
has
significant
health-
lifespan
extending
results
animal
models.
Nevertheless,
it
remains
unclear
if
similar
translate
humans.
A
requirement
translation
development
age-
associated
biomarkers
longitudinal
trials
difficult
not
feasible,
practical,
nor
ethical
when
human
life
span
is
endpoint.
Current
anti-aging
intervention
studies
humans
will
be
covered
within
this
paper.
future
clinical
may
phase
2
3
larger
populations
safety
tolerability
investigated
medication
continues
a
hurdle
for
further
investigations.
