bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2023,
Номер
unknown
Опубликована: Ноя. 5, 2023
Abstract
It
has
been
demonstrated
that
short-term
stress
can
enhance
cellular
responses
and
promote
longevity,
whereas
long-term
shortens
lifespan.
Understanding
the
relationship
between
could
offer
new
insights
into
comprehending
modulating
age-related
diseases.
In
this
study,
we
investigate
using
transcriptomic
metabolomic
analyses
in
yeast
model
system
(
Saccharomyces
cerevisiae
).
We
employed
three
metabolic
treatments:
firstly,
treating
cells
with
threshold
levels
of
benzoic
acid
for
24
hours
(Short-term
[ST]
Stressed
Cells);
secondly,
500
hours,
sub-culturing
every
(Long-term
[LT]
thirdly,
allowing
stressed
to
grow
16
without
any
(Recovered
Cells).
Here,
propose
aging
is
an
evolutionarily
conserved
adaptation
mechanism
response
exposure.
Under
conditions,
prominent
lifespan-extending
metabolites
such
as
trehalose
linked
tumor
suppression
humans,
5’-methylthioadenosine,
were
overexpressed.
contrast,
LT
Cells
activated
genes
those
responsible
epigenetic
regulatory
enzymes
govern
process,
secondary
genes,
heat
shock
proteins
(HSPs)
which
are
associated
cell
damage
but
also
often
aged
cells.
Chronological
lifespan
experiments
showed
lived
a
shorter
compared
ST
Cells.
This
suggests
markers
(eg.
HSPs,
certain
regulators)
expressed
enable
survival
have
effect
reducing
support
hypothesis,
show
exclusively
solely
eukaryotes,
while
significantly
(aging
related)
exhibit
high
conservation
across
all
domains
life,
majority
having
originated
from
bacteria
hinting
at
potential
evolutionary
benefit
aging.
Ageing Research Reviews,
Год журнала:
2023,
Номер
87, С. 101922 - 101922
Опубликована: Март 31, 2023
The
restriction
of
calories,
branched-chain
amino
acids,
and
methionine
have
all
been
shown
to
extend
lifespan
in
model
organisms.
Recently,
glycine
was
found
boost
longevity
genetically
heterogenous
mice.
This
simple
acid
similarly
extends
rats
improves
health
mammalian
models
age-related
disease.
While
compelling
data
indicate
that
is
a
pro-longevity
molecule,
divergent
mechanisms
may
underlie
its
effects
on
aging.
Glycine
abundant
collagen,
building
block
for
glutathione,
precursor
creatine,
an
acceptor
the
enzyme
N-methyltransferase
(GNMT).
A
review
literature
strongly
implicates
GNMT,
which
clears
from
body
by
taking
methyl
group
S-adenosyl-L-methionine
methylating
form
sarcosine.
In
flies,
Gnmt
required
reduced
insulin/insulin-like
growth
factor
1
signaling
dietary
fully
lifespan.
geroprotector
spermidine
requires
upregulate
autophagy
genes
longevity.
Moreover,
overexpression
sufficient
reduce
levels.
Sarcosine,
or
methylglycine,
declines
with
age
multiple
species
capable
inducing
both
vitro
vivo.
Taken
together,
existing
evidence
suggests
prolongs
life
mimicking
activating
autophagy.
Abstract
Methionine
restriction
(MetR)
can
extend
lifespan
and
delay
the
onset
of
aging‐associated
pathologies
in
most
model
organisms.
Previously,
we
showed
that
supplementation
with
metabolite
S
‐adenosyl‐L‐homocysteine
(SAH)
extends
activates
energy
sensor
AMP‐activated
protein
kinase
(AMPK)
budding
yeast
Saccharomyces
cerevisiae
.
However,
mechanism
involved
whether
SAH
metazoan
have
remained
unknown.
Here,
show
reduces
Met
levels
recapitulates
many
physiological
molecular
effects
MetR.
In
yeast,
leads
to
inhibition
target
rapamycin
complex
1
(TORC1)
activation
autophagy.
Furthermore,
Caenorhabditis
elegans
treatment
by
activating
AMPK
providing
benefits
Therefore,
propose
be
used
as
an
intervention
lower
intracellular
confer
Abstract
Aging
is
a
biological
process
along
with
systemic
and
multiple
organ
dysfunction.
It
more
recognized
that
aging
disease
instead
of
single‐organ
functional
disorder.
Systemic
plays
profound
role
in
diseases
including
neurodegenerative
diseases,
cardiovascular
malignant
diseases.
Aged
organs
communicate
other
accelerate
aging.
Skeletal
muscle,
heart,
bone
marrow,
skin,
liver
each
through
organ–organ
crosstalk.
The
crosstalk
can
be
mediated
by
metabolites
lipids,
glucose,
short‐chain
fatty
acids
(SCFA),
inflammatory
cytokines,
exosomes.
Metabolic
disorders
hyperglycemia,
hyperinsulinemia,
hypercholesterolemia
caused
chronic
hallmarks
leads
to
the
destruction
hemostasis,
causes
release
senescence‐associated
secretory
phenotype
(SASP),
imbalance
microbiota
composition.
Released
factors
further
aggregate
senescence,
which
promotes
solid
organs.
Targeting
senescence
or
delaying
emerging
as
critical
health
strategy
for
solving
age‐related
especially
old
population.
In
current
review,
we
will
delineate
mechanisms
provide
therapeutic
targets
Nutrition Research and Practice,
Год журнала:
2023,
Номер
17(4), С. 597 - 597
Опубликована: Янв. 1, 2023
Healthy
aging
can
be
defined
as
an
extended
lifespan
and
health
span.
Nutrition
has
been
regarded
important
factor
in
healthy
aging,
because
nutrients,
bioactive
food
components,
diets
have
demonstrated
beneficial
effects
on
hallmarks
such
oxidative
stress,
mitochondrial
function,
apoptosis
autophagy,
genomic
stability,
immune
function.
also
plays
a
role
epigenetic
regulation
of
gene
expression,
DNA
methylation
is
the
most
extensively
investigated
phenomenon
aging.
Interestingly,
age-associated
modulated
by
one-carbon
metabolism
or
inhibition
methyltransferases.
One-carbon
ultimately
controls
balance
between
universal
methyl
donor
S-adenosylmethionine
methyltransferase
inhibitor
S-adenosylhomocysteine.
Water-soluble
B-vitamins
folate,
vitamin
B6,
B12
serve
coenzymes
for
multiple
steps
metabolism,
whereas
methionine,
choline,
betaine,
serine
act
donors.
Thus,
these
nutrients
modify
subsequently
alter
physiologic
pathologic
processes.
We
cannot
elude
per
se
but
we
may
at
least
change
methylation,
which
could
mitigate
diseases
disorders.
Biochemical and Biophysical Research Communications,
Год журнала:
2024,
Номер
719, С. 150027 - 150027
Опубликована: Май 9, 2024
Aging
is
a
complex,
degenerative
process
associated
with
various
metabolic
abnormalities.
Ginsenosides
(GS)
the
main
active
components
of
Panax
ginseng,
which
has
anti-aging
effects
and
improves
metabolism.
However,
effect
mechanism
GS
in
middle-aged
mice
not
been
elucidated.
In
this
study,
after
3-month
treatment
significantly
improved
grip
strength,
fatigue
resistance,
cognitive
indices,
cardiac
function
15-month-old
mice.
Meanwhile,
reduced
fat
content
obviously
inhibited
histone
H2AX
phosphorylation
at
Ser
139
(γ-H2AX),
marker
DNA
damage
major
organs,
especially
heart
liver.
Further,
correlation
analysis
serum
metabolomics
combined
aging
phenotype
suggested
that
myo-inositol
(MI)
upregulated
by
was
positively
correlated
left
ventricular
ejection
fraction
(LVEF)
fractional
shortening
(LVFS),
indicators
function.
More
importantly,
liver
tissue
metabolomic
showed
increased
MI
promoting
synthesis
pathway
from
phosphatidylcholine
(PC)
to
for
inhibition
aging.
Finally,
we
proved
percentage
senescence-associated
β-galactosidase
staining,
γ-H2AX
immunofluorescence
p21
expression,
production
reactive
oxygen
species
H
iScience,
Год журнала:
2022,
Номер
25(11), С. 105304 - 105304
Опубликована: Окт. 7, 2022
Epigenetic
aging
clocks
are
computational
models
that
use
DNA
methylation
sites
to
predict
age.
Since
cheek
swabs
non-invasive
and
painless,
collecting
from
buccal
tissue
is
highly
desirable.
Here,
we
review
11
existing
have
been
applied
tissue.
Two
of
these
were
exclusively
trained
on
adults
and,
while
moderately
accurate,
not
used
capture
health-relevant
differences
in
epigenetic
Using
130
common
CpGs
utilized
by
two
or
more
clocks,
generate
a
proof-of-concept
predictor
an
adult
methylomic
dataset.
In
addition
accurately
estimating
age
(r
=
0.95
mean
absolute
error
3.88
years),
this
clock
predicted
Down
syndrome
subjects
significantly
older
relative
controls.
A
literature
database
CpG-associated
genes
identified
numerous
(e.g.,
CLOCK,
ELOVL2,
VGF)
molecules
alpha-linolenic
acid,
glycine,
spermidine)
reported
influence
lifespan
and/or
age-related
disease
model
organisms.