Frontiers in Immunology,
Год журнала:
2019,
Номер
10
Опубликована: Окт. 30, 2019
Inflammation
aims
to
restore
tissue
homeostasis
after
injury
or
infection.
Age-related
decline
of
causes
a
physiological
low-grade
chronic
inflammatory
phenotype
known
as
inflammaging
that
is
involved
in
many
age-related
diseases.
Activation
tryptophan
(Trp)
metabolism
along
the
kynurenine
(Kyn)
pathway
prevents
hyperinflammation
and
induces
long-term
immune
tolerance.
Systemic
Trp
Kyn
levels
change
upon
aging
Moreover,
modulation
can
either
aggravate
prevent
inflammaging-related
In
this
review,
we
discuss
how
Kyn/Trp
activation
necessary
control
alters
functioning
other
metabolic
faiths
including
metabolites,
microbiota-derived
indoles
nicotinamide
adenine
dinucleotide
(NAD+).
We
explore
potential
ratio
biomarker
intervening
might
extend
health-
lifespan.
Frontiers in Immunology,
Год журнала:
2018,
Номер
8
Опубликована: Янв. 9, 2018
The
immune
system
is
the
most
important
protective
physiological
of
organism.
It
has
many
connections
with
other
systems
and
is,
in
fact,
often
considered
as
part
larger
neuro-endocrine-immune
axis.
Most
experimental
data
on
changes
aging
show
a
decline
parameters
when
compared
to
young
healthy
subjects.
bulk
these
termed
immunosenescence.
Immunosenescence
been
for
some
time
detrimental
because
it
leads
subclinical
accumulation
proinflammatory
factors
inflamm-aging.
Together,
immunosenescence
inflamm-aging
are
suggested
stand
at
origin
diseases
elderly,
such
infections,
cancer,
autoimmune
disorders,
chronic
inflammatory
diseases.
However,
an
increasing
number
immune-gerontologists
have
challenged
this
negative
interpretation
respect
its
significance
aging-related
alterations
system.
If
one
considers
from
evolutionary
perspective,
they
can
be
viewed
preferably
adaptive
or
remodeling
rather
than
solely
detrimental.
Whereas
conceivable
that
global
may
lead
various
diseases,
also
obvious
needed
extended
survival/longevity.
Recent
cumulative
suggest
that,
without
existence
immunosenescence/inflamm-aging
duo
(representing
two
sides
same
phenomenon),
human
longevity
would
greatly
shortened.
This
review
summarizes
recent
dynamic
reassessment
aging.
Accordingly,
attempts
intervene
by
targeting
rejuvenation,
more
suitable
aim
maintain
general
homeostasis
function
appropriately
improving
immune-inflammatory-functions.
International Immunology,
Год журнала:
2020,
Номер
33(3), С. 127 - 148
Опубликована: Дек. 15, 2020
IL-6
is
involved
both
in
immune
responses
and
inflammation,
hematopoiesis,
bone
metabolism
embryonic
development.
plays
roles
chronic
inflammation
(closely
related
to
inflammatory
diseases,
autoimmune
diseases
cancer)
even
the
cytokine
storm
of
corona
virus
disease
2019
(COVID-19).
Acute
during
response
wound
healing
a
well-controlled
response,
whereas
are
uncontrolled
responses.
Non-immune
cells,
cytokines
such
as
IL-1β,
tumor
necrosis
factor
alpha
(TNFα)
transcription
factors
nuclear
factor-kappa
B
(NF-κB)
signal
transducer
activator
3
(STAT3)
play
central
inflammation.
Synergistic
interactions
between
NF-κB
STAT3
induce
hyper-activation
followed
by
production
various
cytokines.
Because
an
target,
simultaneous
activation
non-immune
cells
triggers
positive
feedback
loop
IL-6-STAT3
axis.
This
called
amplifier
(IL-6
Amp)
key
player
local
initiation
model,
which
states
that
initiators,
senescence,
obesity,
stressors,
infection,
injury
smoking,
trigger
promoting
cells.
model
counters
dogma
holds
autoimmunity
oncogenesis
triggered
breakdown
tissue-specific
tolerance
oncogenic
mutations,
respectively.
The
Amp
activated
variety
demonstrating
axis
critical
target
for
treating
diseases.
Geroscience,
the
new
interdisciplinary
field
that
aims
to
understand
relationship
between
aging
and
chronic
age-related
diseases
(ARDs)
geriatric
syndromes
(GSs),
is
based
on
epidemiological
evidence
experimental
data
major
risk
factor
for
such
pathologies
assumes
ARDs/GSs
share
a
common
set
of
basic
biological
mechanisms.
A
consequence
primary
target
medicine
combat
instead
any
single
ARD/GSs
one
by
one,
as
favored
fragmentation
into
hundreds
specialties
sub-specialties.
If
same
molecular
cellular
mechanisms
underpin
both
ARDs/GSs,
question
emerges:
which
difference,
if
any,
ARDs/GSs?
The
hypothesis
ARDs
GSs
frailty
can
be
conceptualized
accelerated
will
discussed
analyzing
in
particular
frailty,
sarcopenia,
obstructive
pulmonary
disease,
cancer,
neurodegenerative
Alzheimer
Parkinson
well
Down
syndrome
an
example
progeroid
syndrome.
According
this
integrated
view,
become
part
continuum
where
precise
boundaries
do
not
exist
two
extremes
are
represented
centenarians,
who
largely
avoided
or
postponed
most
characterized
decelerated
aging,
patients
suffered
more
severe
their
60s,
70s,
80s
show
signs
respectively.
In
these
extremes,
there
intermediate
trajectories
representing
sort
gray
area.
Thus,
clinically
different,
classical
are,
indeed,
result
peculiar
combinations
alterations
regarding
same,
limited
shared
with
process.
Whether
individual
follow
trajectory
depend
his/her
genetic
background
interacting
lifelong
environmental
lifestyle
factors.
manifestations
it
urgent
identify
markers
capable
distinguishing
chronological
age
subjects
at
higher
developing
GSs.
To
aim,
we
propose
use
DNA
methylation,
N-glycans
profiling,
gut
microbiota
composition
complement
available
disease-specific
markers.
Signal Transduction and Targeted Therapy,
Год журнала:
2023,
Номер
8(1)
Опубликована: Июнь 8, 2023
Abstract
Aging
is
characterized
by
systemic
chronic
inflammation,
which
accompanied
cellular
senescence,
immunosenescence,
organ
dysfunction,
and
age-related
diseases.
Given
the
multidimensional
complexity
of
aging,
there
an
urgent
need
for
a
systematic
organization
inflammaging
through
dimensionality
reduction.
Factors
secreted
senescent
cells,
known
as
senescence-associated
secretory
phenotype
(SASP),
promote
inflammation
can
induce
senescence
in
normal
cells.
At
same
time,
accelerates
immune
resulting
weakened
function
inability
to
clear
cells
inflammatory
factors,
creates
vicious
cycle
senescence.
Persistently
elevated
levels
organs
such
bone
marrow,
liver,
lungs
cannot
be
eliminated
leading
damage
aging-related
Therefore,
has
been
recognized
endogenous
factor
elimination
could
potential
strategy
anti-aging.
Here
we
discuss
at
molecular,
cellular,
organ,
disease
levels,
review
current
aging
models,
implications
cutting-edge
single
cell
technologies,
well
anti-aging
strategies.
Since
preventing
alleviating
diseases
improving
overall
quality
life
are
ultimate
goals
research,
our
highlights
critical
features
mechanisms
along
with
latest
developments
future
directions
providing
theoretical
foundation
novel
practical
