Circulation Research,
Journal Year:
2018,
Volume and Issue:
123(7), P. 868 - 885
Published: Sept. 13, 2018
The
sirtuin
family
of
nicotinamide
adenine
dinucleotide–dependent
deacylases
(SIRT1–7)
are
thought
to
be
responsible,
in
large
part,
for
the
cardiometabolic
benefits
lean
diets
and
exercise
when
upregulated
can
delay
key
aspects
aging.
SIRT1,
example,
protects
against
a
decline
vascular
endothelial
function,
metabolic
syndrome,
ischemia-reperfusion
injury,
obesity,
cardiomyopathy,
SIRT3
is
protective
dyslipidemia
injury.
With
increasing
age,
however,
dinucleotide
levels
activity
steadily
decrease,
further
exacerbated
by
obesity
sedentary
lifestyles.
Activation
sirtuins
or
repletion
induces
angiogenesis,
insulin
sensitivity,
other
health
wide
range
age-related
cardiovascular
disease
models.
Human
clinical
trials
testing
agents
that
activate
SIRT1
boost
progress
show
promise
their
ability
improve
patients.
Science,
Journal Year:
2015,
Volume and Issue:
350(6265), P. 1208 - 1213
Published: Dec. 3, 2015
Nicotinamide
adenine
dinucleotide
(NAD(+))
is
a
coenzyme
found
in
all
living
cells.
It
serves
both
as
critical
for
enzymes
that
fuel
reduction-oxidation
reactions,
carrying
electrons
from
one
reaction
to
another,
and
cosubstrate
other
such
the
sirtuins
poly(adenosine
diphosphate-ribose)
polymerases.
Cellular
NAD(+)
concentrations
change
during
aging,
modulation
of
usage
or
production
can
prolong
health
span
life
span.
Here
we
review
factors
regulate
discuss
how
supplementation
with
precursors
may
represent
new
therapeutic
opportunity
aging
its
associated
disorders,
particularly
neurodegenerative
diseases.
Cell Metabolism,
Journal Year:
2016,
Volume and Issue:
24(6), P. 795 - 806
Published: Oct. 27, 2016
Highlights•NMN
suppresses
age-associated
body
weight
gain
and
enhances
energy
metabolism•NMN
improves
insulin
sensitivity,
eye
function,
other
features
with
no
toxicity•NMN
prevents
gene
expression
changes
in
a
tissue-specific
manner•NMN
is
an
effective
anti-aging
intervention
that
could
be
translated
to
humansSummaryNAD+
availability
decreases
age
certain
disease
conditions.
Nicotinamide
mononucleotide
(NMN),
key
NAD+
intermediate,
has
been
shown
enhance
biosynthesis
ameliorate
various
pathologies
mouse
models.
In
this
study,
we
conducted
12-month-long
NMN
administration
regular
chow-fed
wild-type
C57BL/6N
mice
during
their
normal
aging.
Orally
administered
was
quickly
utilized
synthesize
tissues.
Remarkably,
effectively
mitigates
physiological
decline
mice.
Without
any
obvious
toxicity
or
deleterious
effects,
suppressed
gain,
enhanced
metabolism,
promoted
physical
activity,
improved
sensitivity
plasma
lipid
profile,
ameliorated
function
pathophysiologies.
Consistent
these
phenotypes,
prevented
metabolic
organs
mitochondrial
oxidative
metabolism
mitonuclear
protein
imbalance
skeletal
muscle.
These
effects
of
highlight
the
preventive
therapeutic
potential
intermediates
as
interventions
humans.Graphical
abstract
Signal Transduction and Targeted Therapy,
Journal Year:
2020,
Volume and Issue:
5(1)
Published: Oct. 7, 2020
Abstract
Nicotinamide
adenine
dinucleotide
(NAD
+
)
and
its
metabolites
function
as
critical
regulators
to
maintain
physiologic
processes,
enabling
the
plastic
cells
adapt
environmental
changes
including
nutrient
perturbation,
genotoxic
factors,
circadian
disorder,
infection,
inflammation
xenobiotics.
These
effects
are
mainly
achieved
by
driving
effect
of
NAD
on
metabolic
pathways
enzyme
cofactors
transferring
hydrogen
in
oxidation-reduction
reactions.
Besides,
multiple
-dependent
enzymes
involved
physiology
either
post-synthesis
chemical
modification
DNA,
RNA
proteins,
or
releasing
second
messenger
cyclic
ADP-ribose
(cADPR)
NAADP
.
Prolonged
disequilibrium
metabolism
disturbs
physiological
functions,
resulting
diseases
diseases,
cancer,
aging
neurodegeneration
disorder.
In
this
review,
we
summarize
recent
advances
our
understanding
molecular
mechanisms
-regulated
responses
stresses,
contribution
deficiency
various
via
manipulating
cellular
communication
networks
potential
new
avenues
for
therapeutic
intervention.
