Metabolic
dysregulation
represents
one
of
the
major
driving
forces
in
aging.
Although
multiple
genetic
and
pharmacological
manipulations
are
known
to
extend
longevity
model
organisms,
aging
is
a
complex
trait,
targeting
one’s
own
genes
may
be
insufficient
prevent
age-dependent
deterioration.
An
alternative
strategy
could
use
enzymes
from
other
species
reverse
age-associated
metabolic
changes.
In
this
review,
we
discuss
set
lower
organisms
that
have
been
shown
affect
various
parameters
linked
age-related
processes.
These
include
modulators
steady-state
levels
amino
acids
(METase,
ASNase,
ADI),
NADPH/NADP
+
and/or
reduced
form
coenzyme
Q
(CoQH
2
)/CoQ
redox
potentials
(NDI1,
AOX,
Lb
NOX,
TPNOX,
Ec
STH,
RquA,
LOXCAT,
Grubraw,
ScURA),
GSH
(StGshF),
mitochondrial
membrane
potential
(mtON
mito-dR),
or
reactive
oxygen
(DAAO
KillerRed-SOD1).
We
propose
leveraging
non-mammalian
an
untapped
resource
can
used
delay
diseases.
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.
Abstract
Aging
and
cancer
exhibit
apparent
links
that
we
will
examine
in
this
review.
The
null
hypothesis
aging
coincide
because
both
are
driven
by
time,
irrespective
of
the
precise
causes,
can
be
confronted
with
idea
share
common
mechanistic
grounds
referred
to
as
‘hallmarks’.
Indeed,
several
hallmarks
also
contribute
carcinogenesis
tumor
progression,
but
some
molecular
cellular
characteristics
may
reduce
probability
developing
lethal
cancer,
perhaps
explaining
why
very
old
age
(>
90
years)
is
accompanied
a
reduced
incidence
neoplastic
diseases.
We
discuss
possibility
process
itself
causes
meaning
time-dependent
degradation
supracellular
functions
accompanies
produces
byproduct
or
‘age-associated
disease’.
Conversely,
its
treatment
erode
health
drive
process,
has
dramatically
been
documented
for
survivors
diagnosed
during
childhood,
adolescence,
young
adulthood.
conclude
connected
superior
including
endogenous
lifestyle
factors,
well
bidirectional
crosstalk,
together
render
not
only
risk
factor
an
important
parameter
must
considered
therapeutic
decisions.
It
has
been
reported
that
hyaluronic
acid
(HA)
with
a
35
kDa
molecular
weight
(HA35)
acts
biologically
to
protect
tissue
from
injury,
but
its
biological
properties
are
not
yet
fully
characterized.
This
study
aimed
evaluate
the
cellular
effects
and
biodistribution
of
HA35
compared
HA
1600
(HA1600).
We
assessed
HA1600
on
cell
migration,
NO
ROS
generation,
gene
expression
in
cultured
macrophages,
microglia,
lymphocytes.
was
separately
radiolabeled
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Июль 7, 2024
SUMMARY
Health
is
strongly
affected
by
aging
and
lifespan-modulating
interventions,
but
the
molecular
mechanisms
of
mortality
regulation
remain
unclear.
Here,
we
conducted
an
RNA-seq
analysis
mice
subjected
to
20
compound
treatments
in
Interventions
Testing
Program
(ITP).
By
integrating
it
with
data
from
over
4,000
rodent
tissues
representing
responses
genetic,
pharmacological,
dietary
interventions
established
survival
data,
developed
robust
multi-tissue
transcriptomic
biomarkers
mortality,
capable
quantifying
change
lifespan
both
short-lived
long-lived
models.
These
tools
were
further
extended
single-cell
human
demonstrating
common
across
cell
types
species.
Via
a
network
analysis,
identified
annotated
26
co-regulated
modules
longevity
tissues,
interpretable
module-specific
clocks
that
capture
aging-
mortality-associated
phenotypes
functional
components,
including,
among
others,
inflammatory
response,
mitochondrial
function,
lipid
metabolism,
extracellular
matrix
organization.
captured
characterized
acceleration
biological
age
induced
progeria
models
chronic
diseases
rodents
humans.
They
also
revealed
rejuvenation
heterochronic
parabiosis,
early
embryogenesis,
cellular
reprogramming,
highlighting
universal
signatures
shared
age-related
disease.
included
Cdkn1a
Lgals3
,
whose
plasma
levels
demonstrated
strong
association
all-cause
disease
incidence
risk
factors,
such
as
obesity
hypertension.
Overall,
this
study
uncovers
hallmarks
mammalian
organs,
types,
species
rejuvenation,
exposing
fundamental
longevity.
Abstract
Osteoarthritis
(OA)
poses
a
significant
challenge
in
orthopedics.
Inflammatory
pathways
are
regarded
as
central
mechanisms
the
onset
and
progression
of
OA.
Growing
evidence
suggests
that
senescence
acts
mediator
inflammation-induced
Given
lack
effective
treatments
for
OA,
there
is
an
urgent
need
clearer
understanding
its
pathogenesis.
In
this
review,
we
systematically
summarize
cross-talk
between
cellular
inflammation
We
begin
by
focusing
on
hallmarks
senescence,
summarizing
supports
relationship
inflammation.
then
discuss
interaction
inflammation,
including
senescence-associated
secretory
phenotypes
(SASP)
effects
pro-
anti-inflammatory
interventions
senescence.
Additionally,
focus
various
types
cartilage,
subchondral
bone,
synovium,
infrapatellar
fat
pad,
stem
cells,
immune
elucidating
their
impacts
Finally,
highlight
potential
therapies
targeting
senescent
cells
OA
strategy
promoting
cartilage
regeneration.
HA
(hyaluronan)
has
been
considered
in
recent
years
as
a
naturally
occurring
modifiable
gel-like
scaffold
that
the
capability
to
absorb
and
release
drugs
over
an
extended
period
of
time
making
it
suitable
potential
chemotherapeutic
delivery
agent.
Considering
limited
treatment
options
available
glioblastoma,
this
review,
we
discuss
novel
utilisation
ultra-high
molecular
weight
HA-originally
identified
mechanism
for
maintaining
longevity
naked
mole-rat-as
both
protective
extracellular
matrix-optimizing
colloidal
scaffold,
means
deliver
therapy
resected
brain
tumours.
The
unique
properties
form
cross-linked
gel
indicate
future
use
prevention
proliferative-based
inflammation-driven
disease.
