FEBS Journal,
Journal Year:
2018,
Volume and Issue:
286(6), P. 1058 - 1073
Published: Sept. 21, 2018
The
biology
of
aging
is
an
area
intense
research,
and
many
questions
remain
about
how
why
cell
organismal
functions
decline
over
time.
In
mammalian
cells,
genomic
instability
mitochondrial
dysfunction
are
thought
to
be
among
the
primary
drivers
cellular
aging.
This
review
focuses
on
interrelationship
between
in
cells
its
relevance
age‐related
functional
at
molecular
level.
importance
oxidative
stress
key
DNA
damage
response
pathways
discussed,
with
a
special
focus
poly
(
ADP
‐ribose)
polymerase
1,
whose
persistent
activation
depletes
energy
reserves,
leading
dysfunction,
loss
homeostasis,
altered
metabolism.
Elucidation
relationship
instability,
signaling
that
connect
these
pathways/processes
keys
future
research
human
An
important
component
health
preservation
mitophagy,
this
other
areas
particularly
ripe
for
investigation
will
discussed.
Frontiers in Genetics,
Journal Year:
2018,
Volume and Issue:
9
Published: Aug. 23, 2018
Cellular
senescence
is
an
irreversible
growth
arrest
that
occurs
as
a
result
of
different
damaging
stimuli,
including
DNA
damage,
telomere
shortening
and
dysfunction
or
oncogenic
stress.
Senescent
cells
exert
pleotropic
effect
on
development,
tissue
aging
regeneration,
inflammation,
wound
healing
tumor
suppression.
Strategies
to
remove
senescent
from
tissues
preneoplastic
lesions
can
delay
lead
increased
healthspan.
However,
significant
hurdle
in
the
field
has
been
identification
universal
biomarker
facilitates
unequivocal
detection
quantification
cell
types
vitro
vivo.
Mammalian
skin
largest
organ
human
body
consists
compartments.
Skin
provides
physical
barrier
against
harmful
microbes,
toxins
protects
us
ultraviolet
radiation.
Increasing
evidence
suggests
accumulate
chronologically-
photoaged
skin;
may
contribute
age-related
changes
pathologies.
Here,
we
highlight
current
biomarkers
detect
review
their
utility
context
aging.
In
particular,
discuss
efficacy
within
compartments
types,
how
they
myriad
manifestations
Aging and Disease,
Journal Year:
2017,
Volume and Issue:
8(5), P. 628 - 628
Published: Jan. 1, 2017
Aging
is
the
inevitable
time-dependent
decline
in
physiological
organ
function
and
a
major
risk
factor
for
cancer
development.
Due
to
advances
health
care,
hygiene
control
food
availability,
life
expectancy
increasing
population
most
developed
countries
shifting
an
proportion
of
people
at
susceptible
age.
Mechanisms
aging
are
also
found
occur
carcinogenesis,
albeit
with
shared
or
divergent
end-results.
It
now
clear
that
development
either
share
diverge
several
disease
mechanisms.
Such
mechanisms
include
role
genomic
instability,
telomere
attrition,
epigenetic
changes,
loss
proteostasis,
decreased
nutrient
sensing
altered
metabolism,
but
cellular
senescence
stem
cell
function.
Cancer
cells
aged
fundamentally
opposite,
as
can
be
thought
hyperactive
advantageous
mutations,
rapid
division
increased
energy
consumption,
while
hypoactive
accumulated
disadvantageous
inability
ability
production
consumption.
Nonetheless,
tightly
interconnected
many
same
strategies
drugs
may
used
target
both,
other
cases
antagonistic
pleiotrophy
come
into
effect
inhibition
one
activation
other.
considered
disease,
though
underpinning
two
processes
remain
unclear.
Better
understanding
pathways
needed.
Journal of the American College of Cardiology,
Journal Year:
2020,
Volume and Issue:
75(8), P. 919 - 930
Published: Feb. 24, 2020
Aging
is
the
main
risk
factor
for
vascular
disease
and
ensuing
cardiovascular
cerebrovascular
events,
leading
causes
of
death
worldwide.
In
a
progressively
aging
population,
it
essential
to
develop
early-life
biomarkers
that
efficiently
identify
individuals
who
are
at
high
developing
accelerated
damage,
with
ultimate
goal
improving
primary
prevention
reducing
health
care
socioeconomic
impact
age-related
disease.
Studies
in
experimental
models
humans
have
identified
9
highly
interconnected
hallmark
processes
driving
mammalian
aging.
However,
strategies
extend
span
life
require
understanding
interindividual
differences
age-dependent
functional
decline,
known
as
biological
This
review
summarizes
current
knowledge
on
age
biomarkers,
factors
influencing
aging,
antiaging
interventions,
focus
aspects
process
its
related
manifestations.
Nature Communications,
Journal Year:
2019,
Volume and Issue:
10(1)
Published: Nov. 21, 2019
Abstract
Metabolic
dysfunction
is
a
primary
feature
of
Werner
syndrome
(WS),
human
premature
aging
disease
caused
by
mutations
in
the
gene
encoding
(WRN)
DNA
helicase.
WS
patients
exhibit
severe
metabolic
phenotypes,
but
underlying
mechanisms
are
not
understood,
and
whether
deficit
can
be
targeted
for
therapeutic
intervention
has
been
determined.
Here
we
report
impaired
mitophagy
depletion
NAD
+
,
fundamental
ubiquitous
molecule,
patient
samples
invertebrate
models.
WRN
regulates
transcription
key
biosynthetic
enzyme
nicotinamide
nucleotide
adenylyltransferase
1
(NMNAT1).
repletion
restores
profiles
improves
mitochondrial
quality
through
DCT-1
ULK-1-dependent
mitophagy.
At
organismal
level,
remarkably
extends
lifespan
delays
accelerated
aging,
including
stem
cell
dysfunction,
Caenorhabditis
elegans
Drosophila
melanogaster
models
WS.
Our
findings
suggest
that
mediated
function
mitophagy,
bolstering
cellular
levels
counteracts
phenotypes.
