International Journal of Molecular Sciences,
Год журнала:
2019,
Номер
20(5), С. 1223 - 1223
Опубликована: Март 11, 2019
Aging
and
various
age-related
diseases
are
associated
with
reductions
in
melatonin
secretion,
proinflammatory
changes
the
immune
system,
a
deteriorating
circadian
sirtuin-1
(SIRT1)
activity.
In
non-tumor
cells,
several
effects
of
abolished
by
inhibiting
SIRT1,
indicating
mediation
SIRT1.
Melatonin
is,
addition
to
its
antioxidant
roles,
an
stimulatory
agent.
However,
it
can
act
as
either
pro-
or
anti-inflammatory
regulator
context-dependent
way.
stimulate
release
cytokines
other
mediators,
but
also,
under
different
conditions,
suppress
inflammation-promoting
processes
such
NO
release,
activation
cyclooxygenase-2,
inflammasome
NLRP3,
gasdermin
D,
toll-like
receptor-4
mTOR
signaling,
cytokine
SASP
(senescence-associated
secretory
phenotype),
amyloid-β
toxicity.
It
also
activates
network,
which
SIRT1
activation,
upregulation
Nrf2
downregulation
NF-κB,
IL-4
IL-10
involved.
A
perhaps
crucial
action
may
be
promotion
macrophage
microglia
polarization
favor
phenotype
M2.
addition,
many
factors
networks
subject
regulation
microRNAs
that
target
mRNAs
respective
upregulate
them
targeting
their
inhibitor
proteins.
Signal Transduction and Targeted Therapy,
Год журнала:
2022,
Номер
7(1)
Опубликована: Дек. 16, 2022
Aging
is
a
gradual
and
irreversible
pathophysiological
process.
It
presents
with
declines
in
tissue
cell
functions
significant
increases
the
risks
of
various
aging-related
diseases,
including
neurodegenerative
cardiovascular
metabolic
musculoskeletal
immune
system
diseases.
Although
development
modern
medicine
has
promoted
human
health
greatly
extended
life
expectancy,
aging
society,
variety
chronic
diseases
have
gradually
become
most
important
causes
disability
death
elderly
individuals.
Current
research
on
focuses
elucidating
how
endogenous
exogenous
stresses
(such
as
genomic
instability,
telomere
dysfunction,
epigenetic
alterations,
loss
proteostasis,
compromise
autophagy,
mitochondrial
cellular
senescence,
stem
exhaustion,
altered
intercellular
communication,
deregulated
nutrient
sensing)
participate
regulation
aging.
Furthermore,
thorough
pathogenesis
to
identify
interventions
that
promote
longevity
caloric
restriction,
microbiota
transplantation,
nutritional
intervention)
clinical
treatment
methods
for
(depletion
senescent
cells,
therapy,
antioxidative
anti-inflammatory
treatments,
hormone
replacement
therapy)
could
decrease
incidence
turn
healthy
longevity.
Archives of Disease in Childhood,
Год журнала:
2020,
Номер
106(5), С. 429 - 439
Опубликована: Дек. 1, 2020
In
contrast
to
other
respiratory
viruses,
children
have
less
severe
symptoms
when
infected
with
the
novel
acute
syndrome
coronavirus
2
(SARS-CoV-2).
this
review,
we
discuss
proposed
hypotheses
for
age-related
difference
in
severity
of
disease
2019
(COVID-19).
Factors
explain
COVID-19
and
adults
include
those
that
put
at
higher
risk
protect
children.
The
former
include:
(1)
increase
endothelial
damage
changes
clotting
function;
(2)
density,
increased
affinity
different
distribution
angiotensin
converting
enzyme
receptors
transmembrane
serine
protease
2;
(3)
pre-existing
antibodies
(including
antibody-dependent
enhancement)
T
cells;
(4)
immunosenescence
inflammaging,
including
effects
chronic
cytomegalovirus
infection;
(5)
a
prevalence
comorbidities
associated
(6)
lower
levels
vitamin
D.
might
differences
innate
adaptive
immunity;
more
frequent
recurrent
concurrent
infections;
immunity
coronaviruses;
microbiota;
melatonin;
protective
off-target
live
vaccines
(7)
intensity
exposure
SARS-CoV-2.
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
