Cellular and Molecular Life Sciences,
Journal Year:
2023,
Volume and Issue:
80(7)
Published: June 24, 2023
Abstract
Ageing
is
characterized
by
the
progressive
loss
of
cellular
homeostasis,
leading
to
an
overall
decline
organism’s
fitness.
In
brain,
ageing
highly
associated
with
cognitive
and
neurodegenerative
diseases.
With
rise
in
life
expectancy,
characterizing
brain
process
becomes
fundamental
for
developing
therapeutic
interventions
against
increased
incidence
age-related
diseases
aim
increase
human
span
and,
more
importantly,
health
span.
this
review,
we
start
introducing
molecular/cellular
hallmarks
their
impact
on
cell
populations.
Subsequently,
assess
emerging
evidence
how
systemic
translates
into
ageing.
Finally,
revisit
mainstream
novel
rejuvenating
strategies,
discussing
most
successful
ones
delaying
related
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: March 14, 2023
Abstract
The
ageing
process
is
a
systemic
decline
from
cellular
dysfunction
to
organ
degeneration,
with
more
predisposition
deteriorated
disorders.
Rejuvenation
refers
giving
aged
cells
or
organisms
youthful
characteristics
through
various
techniques,
such
as
reprogramming
and
epigenetic
regulation.
great
leaps
in
rejuvenation
prove
that
not
one-way
street,
many
rejuvenative
interventions
have
emerged
delay
even
reverse
the
process.
Defining
mechanism
by
which
roadblocks
signaling
inputs
influence
complex
programs
essential
for
understanding
developing
strategies.
Here,
we
discuss
intrinsic
extrinsic
factors
counteract
cell
rejuvenation,
targeted
core
mechanisms
involved
this
Then,
critically
summarize
latest
advances
state-of-art
strategies
of
rejuvenation.
Various
methods
also
provide
insights
treating
specific
ageing-related
diseases,
including
reprogramming,
removal
senescence
(SCs)
suppression
senescence-associated
secretory
phenotype
(SASP),
metabolic
manipulation,
stem
cells-associated
therapy,
dietary
restriction,
immune
heterochronic
transplantation,
etc.
potential
applications
therapy
extend
cancer
treatment.
Finally,
analyze
detail
therapeutic
opportunities
challenges
technology.
Deciphering
will
further
into
anti-ageing
disease
treatment
clinical
settings.
Translational Neurodegeneration,
Journal Year:
2024,
Volume and Issue:
13(1)
Published: Feb. 20, 2024
Abstract
Brain
aging
is
a
recognized
risk
factor
for
neurodegenerative
diseases
like
Alzheimer's
disease,
Parkinson's
and
amyotrophic
lateral
sclerosis
(ALS,
Lou
Gehrig's
disease),
but
the
intricate
interplay
between
brain
pathogenesis
of
these
conditions
remains
inadequately
understood.
Cellular
senescence
considered
to
contribute
cellular
dysfunction
inflammaging.
According
threshold
theory
senescent
cell
accumulation,
vulnerability
associated
with
rates
generation
clearance
within
brain.
Given
role
microglia
in
eliminating
cells,
accumulation
may
lead
acceleration
aging,
contributing
inflammaging
increased
diseases.
In
this
review,
we
propose
idea
that
microglia,
which
notably
vulnerable
could
potentially
serve
as
central
catalyst
progression
The
are
emerging
promising
target
mitigating
Science Advances,
Journal Year:
2024,
Volume and Issue:
10(15)
Published: April 12, 2024
Aging
skin,
vulnerable
to
age-related
defects,
is
poor
in
wound
repair.
Metabolic
regulation
accumulated
senescent
cells
(SnCs)
with
aging
essential
for
tissue
homeostasis,
and
adequate
ATP
important
cell
activation
aged
Strategies
metabolism
intervention
hold
prospects
therapeutic
advances.
Here,
we
found
energy
metabolic
changes
skin
from
patients
mice.
Our
data
show
that
metformin
engineered
EV
(Met-EV)
can
enhance
mouse
repair,
as
well
ameliorate
cellular
senescence
restore
dysfunctions.
Notably,
was
remodeled
reduced
glycolysis
enhanced
OXPHOS
after
Met-EV
treatment.
We
rescue
senescence-induced
mitochondria
dysfunctions
mitophagy
suppressions,
indicating
the
role
of
remodeling
mitochondrial
functions
via
production
results
reveal
mechanism
SnCs
rejuvenation
by
suggest
disturbed
metabolism,
be
a
potential
target
facilitating
Archives of Toxicology,
Journal Year:
2024,
Volume and Issue:
98(8), P. 2393 - 2408
Published: May 15, 2024
Increasing
evidence
has
revealed
that
cellular
senescence
drives
NDs,
including
Alzheimer's
disease
(AD)
and
Parkinson's
disease.
Different
senescent
cell
populations
secrete
senescence-associated
secretory
phenotypes
(SASP),
matrix
metalloproteinase-3,
interleukin
(IL)-1α,
IL-6,
IL-8,
which
can
harm
adjacent
microglia.
Moreover,
these
cells
possess
high
expression
levels
of
hallmarks
(p16
p21)
elevated
β-galactosidase
activity
in
vitro
vivo
ND
models.
These
contribute
to
the
deposition
β-amyloid
tau-protein
tangles.
Selective
clearance
SASP
regulation
by
inhibiting
p38/mitogen-activated
protein
kinase
nuclear
factor
kappa
B
signaling
attenuate
load
prevent
tangle
deposition,
thereby
improving
cognitive
performance
AD
mouse
In
addition,
telomere
shortening,
a
biomarker,
is
associated
with
increased
risks.
Telomere
dysfunction
causes
senescence,
stimulating
tumor
necrosis
factor-α,
IL-1β
secretions.
The
forced
telomerase
activators
prevents
yielding
considerable
neuroprotective
effects.
This
review
elucidates
mechanism
pathogenesis,
suggesting
strategies
eliminate
or
restore
normal
phenotype
for
treating
such
diseases.
Nature Ecology & Evolution,
Journal Year:
2024,
Volume and Issue:
8(6), P. 1140 - 1153
Published: April 15, 2024
Regulation
of
gene
expression
is
arguably
the
main
mechanism
underlying
phenotypic
diversity
tissues
within
and
between
species.
Here
we
assembled
an
extensive
transcriptomic
dataset
covering
8
across
20
bilaterian
species
performed
analyses
using
a
symmetric
phylogeny
that
allowed
combined
parallel
investigation
evolution
vertebrates
insects.
We
specifically
focused
on
widely
conserved
ancestral
genes,
identifying
strong
cores
pan-bilaterian
tissue-specific
genes
even
larger
groups
diverged
to
define
vertebrate
insect
tissues.
Systematic
inferences
tissue-specificity
gains
losses
show
nearly
half
all
have
been
recruited
into
transcriptomes.
This
occurred
during
both
ancient
and,
especially,
recent
evolution,
with
several
being
associated
emergence
unique
phenotypes
(for
example,
novel
cell
types).
Such
pervasive
tissue
specificity
was
linked
duplication
coupled
specialization
one
copies,
revealing
unappreciated
prolonged
effect
whole-genome
duplications
evolution.
A
analysis
reveals
were
closely
in
diversification
types.
