Journal of Biomedical Science,
Год журнала:
2019,
Номер
26(1)
Опубликована: Май 11, 2019
Nicotinamide
adenine
dinucleotide
(NAD)
is
an
important
coenzyme
that
participates
in
various
energy
metabolism
pathways,
including
glycolysis,
β-oxidation,
and
oxidative
phosphorylation.
Besides,
it
a
required
cofactor
for
post-translational
modifications
such
as
ADP-ribosylation
deacetylation
by
poly
(ADP-ribose)
polymerases
(PARPs)
sirtuins,
respectively.
Thus,
NAD
regulates
metabolism,
DNA
damage
repair,
gene
expression,
stress
response
through
these
enzymes.
Numerous
studies
have
shown
levels
decrease
with
aging
under
disturbed
nutrient
conditions,
obesity.
Additionally,
decline
closely
related
to
the
development
of
metabolic
disorders,
diabetes
fatty
liver
disease.
In
addition,
many
revealed
administration
precursors,
nicotinamide
mononucleotide
(NMN)
riboside
(NR),
efficiently
increase
tissues
prevent
diseases.
These
precursors
are
contained
natural
foods,
cow
milk,
vegetables,
meats.
Therefore,
altered
can
be
practical
target
nutritional
intervention.
Recently,
several
human
clinical
trials
using
been
conducted
investigate
safety,
pharmacokinetics,
efficacy
against
disorders
glucose
intolerance.
this
review,
we
summarize
current
knowledge
on
implications
diseases
discuss
outcomes
recent
trials.
Signal Transduction and Targeted Therapy,
Год журнала:
2020,
Номер
5(1)
Опубликована: Окт. 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.
Circulation Research,
Год журнала:
2018,
Номер
123(7), С. 868 - 885
Опубликована: Сен. 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.
Journal of Hematology & Oncology,
Год журнала:
2020,
Номер
13(1)
Опубликована: Ноя. 10, 2020
Immunosenescence
is
a
process
of
immune
dysfunction
that
occurs
with
age
and
includes
remodeling
lymphoid
organs,
leading
to
changes
in
the
function
elderly,
which
closely
related
development
infections,
autoimmune
diseases,
malignant
tumors.
T
cell-output
decline
an
important
feature
immunosenescence
as
well
production
senescence-associated
secretory
phenotype,
increased
glycolysis,
reactive
oxygen
species.
Senescent
cells
exhibit
abnormal
phenotypes,
including
downregulation
CD27,
CD28,
upregulation
CD57,
killer
cell
lectin-like
receptor
subfamily
G,
Tim-3,
Tight,
cytotoxic
T-lymphocyte-associated
protein
4,
are
tightly
The
role
tumors
sophisticated:
many
factors
involved
include
cAMP,
glucose
competition,
oncogenic
stress
tumor
microenvironment,
can
induce
senescence
cells,
macrophages,
natural
dendritic
cells.
Accordingly,
these
senescent
could
also
affect
progression.
In
addition,
effect
on
response
checkpoint
blocking
antibody
therapy
so
far
ambiguous
due
low
participation
elderly
cancer
patients
clinical
trials.
Furthermore,
other
senescence-related
interventions
be
possible
genetic
pharmacological
methods,
mTOR
inhibition,
interleukin-7
recombination,
NAD+
activation.
Overall,
this
review
aims
highlight
characteristics
its
impact
immunotherapy,
especially
future
directions
treatment
through
senescence-focused
strategies.
Signal Transduction and Targeted Therapy,
Год журнала:
2021,
Номер
6(1)
Опубликована: Янв. 1, 2021
NAD+
was
discovered
during
yeast
fermentation,
and
since
its
discovery,
important
roles
in
redox
metabolism,
aging,
longevity,
the
immune
system
DNA
repair
have
been
highlighted.
A
deregulation
of
levels
has
associated
with
metabolic
diseases
aging-related
diseases,
including
neurodegeneration,
defective
responses,
cancer.
acts
as
a
cofactor
through
interplay
NADH,
playing
an
essential
role
many
enzymatic
reactions
energy
such
glycolysis,
oxidative
phosphorylation,
fatty
acid
oxidation,
TCA
cycle.
also
plays
deacetylation
by
sirtuins
ADP
ribosylation
damage/repair
PARP
proteins.
Finally,
different
NAD
hydrolase
proteins
consume
while
converting
it
into
ADP-ribose
or
cyclic
counterpart.
Some
these
proteins,
CD38,
seem
to
be
extensively
involved
response.
Since
cannot
taken
directly
from
food,
metabolism
is
essential,
NAMPT
key
enzyme
recovering
nicotinamide
generating
most
cellular
pools.
Because
complex
network
pathways
which
enzyme,
NAMPT,
cancer
understandable.
In
present
work,
we
review
ways
that
they
may
influence
system,
stemness,
some
ongoing
research
on
therapeutic
approaches.
