Bioactive Materials,
Journal Year:
2023,
Volume and Issue:
25, P. 13 - 28
Published: Jan. 19, 2023
Clinical
therapies
developed
for
estrogen-deficiency-driven
postmenopausal
osteoporosis
(PMO)
and
related
diseases,
such
as
bone
degeneration,
show
multiple
adverse
effects
nowadays.
Targeting
senescent
cells
(SnCs)
the
consequent
senescence-associated
secretory
phenotype
(SASP)
with
a
combination
of
dasatinib
quercetin
(DQ)
is
recently
novel
therapy
age-related
diseases.
Herein,
we
found
that
estrogen
deficiency
induced-bone
loss
was
attributed
to
pro-inflammatory
microenvironment
SASP
secretions
accelerated
SnC
accumulation,
especially
mesenchymal
stem
(MSCs)
characterized
by
exhaustion
dysfunction
in
middle
aged
rats.
Systematically
targeting
SnCs
DQ
strikingly
ameliorated
PMO
restored
MSC
function.
Local
administration
morphogenetic
protein
2
(BMP2)
promoted
osteogenic
differentiation
MSCs
rejuvenated
osteoporotic
regeneration.
Our
results
repurposed
an
attractive
treating
Signal Transduction and Targeted Therapy,
Journal Year:
2022,
Volume and Issue:
7(1)
Published: Dec. 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.
Signal Transduction and Targeted Therapy,
Journal Year:
2023,
Volume and Issue:
8(1)
Published: June 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
Signal Transduction and Targeted Therapy,
Journal Year:
2022,
Volume and Issue:
7(1)
Published: Nov. 7, 2022
Abstract
Aging
is
accompanied
by
the
decline
of
organismal
functions
and
a
series
prominent
hallmarks,
including
genetic
epigenetic
alterations.
These
aging-associated
changes
include
DNA
methylation,
histone
modification,
chromatin
remodeling,
non-coding
RNA
(ncRNA)
regulation,
all
which
participate
in
regulation
aging
process,
hence
contribute
to
aging-related
diseases.
Therefore,
understanding
mechanisms
will
provide
new
avenues
develop
strategies
delay
aging.
Indeed,
interventions
based
on
manipulating
have
led
alleviation
or
extension
lifespan
animal
models.
Small
molecule-based
therapies
reprogramming
that
enable
rejuvenation
been
developed
for
ameliorating
reversing
conditions.
In
addition,
adopting
health-promoting
activities,
such
as
caloric
restriction,
exercise,
calibrating
circadian
rhythm,
has
demonstrated
Furthermore,
various
clinical
trials
intervention
are
ongoing,
providing
more
evidence
safety
efficacy
these
therapies.
Here,
we
review
recent
work
outline
advances
age-associated
A
better
critical
roles
epigenetics
process
lead
prevention
human
therapy
Biochemical Pharmacology,
Journal Year:
2023,
Volume and Issue:
211, P. 115522 - 115522
Published: March 28, 2023
Alzheimer's
disease
(AD)
is
one
of
the
most
prevalent
neurodegenerative
diseases
that
affect
millions
people
worldwide,
with
both
prevalence
and
incidence
increasing
age.
It
characterized
by
cognitive
decline
associated,
specifically,
degeneration
cholinergic
neurons.
The
problem
this
even
more
fundamental
as
available
therapies
remain
fairly
limited
mainly
focused
on
symptoms'
relief.
Although
aetiology
remains
elusive,
two
main
pathological
hallmarks
are
described:
i)
presence
neurofibrillary
tangles
formed
unfolded
protein
aggregates
(hyperphosphorylated
Tau
protein)
ii)
extracellular
amyloid-beta
peptide.
Given
complexity
surrounding
pathogenesis
disease,
several
potential
targets
have
been
highlighted
interrelated
upon
its
progression,
such
oxidative
stress
accumulation
metal
ions.
Thus,
advances
made
development
innovative
multitarget
therapeutical
compounds
to
delay
progression
restore
cell
function.
This
review
focuses
ongoing
research
new
insights
emerging
disease-modifying
drugs
for
AD
treatment.
Furthermore,
classical
novel
biomarkers
early
diagnosis
their
role
in
assisting
improvement
targeted
will
also
be
approached.
Journal of Clinical Investigation,
Journal Year:
2022,
Volume and Issue:
132(14)
Published: July 14, 2022
Aging
is
characterized
by
the
accumulation
of
damage
to
macromolecules
and
cell
architecture
that
triggers
a
proinflammatory
state
in
blood
solid
tissues,
termed
inflammaging.
Inflammaging
has
been
implicated
pathogenesis
many
age-associated
chronic
diseases
as
well
loss
physical
cognitive
function.
The
search
for
mechanisms
underlie
inflammaging
focused
initially
on
hallmarks
aging,
but
it
rapidly
expanding
multiple
directions.
Here,
we
discuss
threads
connecting
cellular
senescence
mitochondrial
dysfunction
impaired
mitophagy
DNA
damage,
which
may
act
hub
We
explore
emerging
multi-omics
efforts
aspire
define
complexity
-
identify
molecular
signatures
novel
targets
interventions
aimed
at
counteracting
excessive
inflammation
its
deleterious
consequences
while
preserving
physiological
immune
response.
Finally,
review
evidence
involved
brain
aging
neurodegenerative
diseases.
Our
goal
broaden
research
agenda
with
an
eye
new
therapeutic
opportunities.
Biomolecules,
Journal Year:
2023,
Volume and Issue:
13(4), P. 686 - 686
Published: April 18, 2023
Closely
associated
with
aging
and
age-related
disorders,
cellular
senescence
(CS)
is
the
inability
of
cells
to
proliferate
due
accumulated
unrepaired
damage
irreversible
cell
cycle
arrest.
Senescent
are
characterized
by
their
senescence-associated
secretory
phenotype
that
overproduces
inflammatory
catabolic
factors
hamper
normal
tissue
homeostasis.
Chronic
accumulation
senescent
thought
be
intervertebral
disc
degeneration
(IDD)
in
an
population.
This
IDD
one
largest
age-dependent
chronic
often
neurological
dysfunctions
such
as,
low
back
pain,
radiculopathy,
myelopathy.
(SnCs)
increase
number
aged,
degenerated
discs,
have
a
causative
role
driving
IDD.
review
summarizes
current
evidence
supporting
CS
on
onset
progression
The
discussion
includes
molecular
pathways
involved
as
p53-p21CIP1,
p16INK4a,
NF-κB,
MAPK,
potential
therapeutic
value
targeting
these
pathways.
We
propose
several
mechanisms
including
mechanical
stress,
oxidative
genotoxic
nutritional
deprivation,
stress.
There
still
large
knowledge
gaps
research,
understanding
which
will
provide
opportunities
develop
interventions
treat