Abstract
Over
the
past
five
years,
systemic
NAD
+
(nicotinamide
adenine
dinucleotide)
decline
has
been
accepted
to
be
a
key
driving
force
of
aging
in
field
research.
The
original
version
World
concept
was
proposed
2009,
providing
an
integrated
view
-centric,
regulatory
network
for
mammalian
and
longevity
control.
reformulated
concept,
2.0,
then
2016,
emphasizing
importance
inter-tissue
communications
between
hypothalamus
peripheral
tissues
including
adipose
tissue
skeletal
muscle.
There
significant
progress
our
understanding
nicotinamide
mononucleotide
(NMN),
intermediate,
phosphoribosyltransferase
(NAMPT),
particularly
extracellular
NAMPT
(eNAMPT).
With
these
exciting
developments,
further
3.0,
is
now
proposed,
featuring
multi-layered
feedback
loops
mediated
by
NMN
eNAMPT
Antioxidants,
Год журнала:
2021,
Номер
10(8), С. 1315 - 1315
Опубликована: Авг. 21, 2021
Vitamin
B3
(nicotinic
acid,
niacin)
deficiency
causes
the
systemic
disease
pellagra,
which
leads
to
dermatitis,
diarrhea,
dementia,
and
possibly
death
depending
on
its
severity
duration.
is
used
in
synthesis
of
NAD
Physiological Reviews,
Год журнала:
2023,
Номер
103(3), С. 1693 - 1787
Опубликована: Янв. 5, 2023
Human
skeletal
muscle
demonstrates
remarkable
plasticity,
adapting
to
numerous
external
stimuli
including
the
habitual
level
of
contractile
loading.
Accordingly,
function
and
exercise
capacity
encompass
a
broad
spectrum,
from
inactive
individuals
with
low
levels
endurance
strength
elite
athletes
who
produce
prodigious
performances
underpinned
by
pleiotropic
training-induced
muscular
adaptations.
Our
current
understanding
signal
integration,
interpretation,
output
coordination
cellular
molecular
mechanisms
that
govern
plasticity
across
this
continuum
is
incomplete.
As
such,
training
methods
their
application
largely
rely
on
“trial-and-error”
approach,
experience
practices
successful
coaches
often
providing
bases
for
“post
hoc”
scientific
enquiry
research.
This
review
provides
synopsis
morphological
functional
changes
along
underlying
adaptation
endurance-
resistance-based
training.
These
traits
are
placed
in
context
innate
genetic
interindividual
differences
performance,
special
consideration
given
aging
athletes.
Collectively,
we
provide
comprehensive
overview
response
different
modes
how
such
adaptations
translate
“molecules
medals.”
Cell Communication and Signaling,
Год журнала:
2024,
Номер
22(1)
Опубликована: Май 24, 2024
Abstract
Aging
is
a
complex
and
multifaceted
process
involving
variety
of
interrelated
molecular
mechanisms
cellular
systems.
Phenotypically,
the
biological
aging
accompanied
by
gradual
loss
function
systemic
deterioration
multiple
tissues,
resulting
in
susceptibility
to
aging-related
diseases.
Emerging
evidence
suggests
that
closely
associated
with
telomere
attrition,
DNA
damage,
mitochondrial
dysfunction,
nicotinamide
adenine
dinucleotide
levels,
impaired
macro-autophagy,
stem
cell
exhaustion,
inflammation,
protein
balance,
deregulated
nutrient
sensing,
altered
intercellular
communication,
dysbiosis.
These
age-related
changes
may
be
alleviated
intervention
strategies,
such
as
calorie
restriction,
improved
sleep
quality,
enhanced
physical
activity,
targeted
longevity
genes.
In
this
review,
we
summarise
key
historical
progress
exploration
important
causes
anti-aging
strategies
recent
decades,
which
provides
basis
for
further
understanding
reversibility
phenotypes,
application
prospect
synthetic
biotechnology
therapy
also
prospected.
Nature Communications,
Год журнала:
2024,
Номер
15(1)
Опубликована: Фев. 16, 2024
Abstract
Senescence
of
vascular
smooth
muscle
cells
(VSMCs)
contributes
to
aging-related
cardiovascular
diseases
by
promoting
arterial
remodelling
and
stiffness.
Ferroptosis
is
a
novel
type
regulated
cell
death
associated
with
lipid
oxidation.
Here,
we
show
that
pro-ferroptosis
signaling
drives
VSMCs
senescence
accelerate
NAD
+
loss,
aging.
Pro-ferroptotic
triggered
in
senescent
arteries
aged
mice.
Furthermore,
the
activation
pro-ferroptotic
not
only
induces
loss
but
also
promotes
release
pro-senescent
secretome.
Pharmacological
or
genetic
inhibition
signaling,
ameliorates
senescence,
reduces
stiffness
retards
progression
abdominal
aortic
aneurysm
Mechanistically,
revealed
facilitates
nuclear-cytoplasmic
shuttling
proliferator-activated
receptor-γ
and,
thereby
impeding
nuclear
receptor
coactivator
4-ferrtin
complex-centric
ferritinophagy.
Finally,
activated
correlates
human
proof-of-concept
study.
These
findings
have
significant
implications
for
future
therapeutic
strategies
aiming
eliminate
ferroptosis
senescence-
aging-associated
diseases.
Frontiers in Immunology,
Год журнала:
2024,
Номер
14
Опубликована: Янв. 8, 2024
Neutrophils
are
the
most
abundant
innate
immune
cells.
Multiple
mechanisms
allow
them
to
engage
a
wide
range
of
metabolic
pathways
for
biosynthesis
and
bioenergetics
mediating
biological
processes
such
as
development
in
bone
marrow
antimicrobial
activity
ROS
production
NET
formation,
inflammation
tissue
repair.
We
first
discuss
recent
work
on
neutrophil
functions
regulate
granulopoiesis,
migration
trafficking
well
effector
functions.
then
syndromes
with
impaired
that
influenced
by
genetic
environmental
factors
nutrient
availability
usage.
Here,
we
particularly
focus
role
specific
macronutrients,
glucose,
fatty
acids,
protein,
micronutrients
vitamin
B3,
regulating
biology
how
this
regulation
impacts
host
health.
A
special
section
review
primarily
discusses
ways
deficiencies
could
impact
increase
infection
susceptibility.
emphasize
biochemical
approaches
explore
metabolism
relation
Lastly,
opportunities
challenges
neutrophil-centered
therapeutic
immune-driven
diseases
highlight
unanswered
questions
guide
future
discoveries.
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease,
Год журнала:
2021,
Номер
1868(1), С. 166287 - 166287
Опубликована: Окт. 7, 2021
Oxidative
stress
and
lipid
peroxidation
are
major
causes
of
skin
injury
induced
by
ultraviolet
(UV)
irradiation.
Ferroptosis
is
a
form
regulated
necrosis
driven
iron-dependent
phospholipids
contributes
to
kinds
tissue
injuries.
However,
it
remains
unclear
whether
the
accumulation
peroxides
in
UV
irradiation-induced
could
lead
ferroptosis.
We
generated
mice
model
examine
iron.
Lipid
4-HNE,
oxidative
enzyme
COX2,
DNA
damage
biomarker
8-OHdG,
iron
level
were
increased
skin.
The
was
also
observed
UVB-irradiated
epidermal
keratinocytes
without
actual
ongoing
ferroptotic
cell
death.
triggered
UV-irradiated
stimulated
with
ferric
ammonium
citrate
(FAC)
mimic
overload.
Although
GPX4
protected
UVB-injured
against
death
resulted
from
dysregulation
metabolism
subsequent
increase
ROS,
enduring
constant
UVB
treatment
markedly
sensitized
Nicotinamide
mononucleotide
(NMN)
which
direct
potent
NAD+
precursor
supplement,
rescued
imbalanced
NAD+/NADH
ratio,
recruited
production
GSH
promoted
resistance
GPX4-dependent
manner.
Taken
together,
our
data
suggest
that
NMN
recruits
enhance
GPX4-mediated
ferroptosis
defense
inhibits
damage.
or
inhibitor
might
become
promising
therapeutic
approaches
for
treating
stress-induced
diseases
disorders.
