Abstract
Cellular
senescence
is
a
key
contributor
to
aging
and
aging-related
diseases,
but
its
metabolic
profiles
are
not
well
understood.
Here,
we
performed
systematic
analysis
of
the
features
four
types
cellular
(replication,
irradiation,
reactive
oxygen
species
[ROS],
oncogene)
in
12
cell
lines
using
genome-wide
modeling
meta-analysis.
We
discovered
that
replicative
ROS-induced
share
common
signature,
marked
by
decreased
lipid
metabolism
downregulated
mevalonate
pathway,
while
irradiation
oncogene-induced
exhibit
more
heterogeneity
divergence.
Our
knockout
simulations
showed
enhancing
administrating
for
instance,
could
reverse
alterations
associated
with
human
tissue
aging,
suggesting
potential
anti-aging
or
lifespan-extending
effect.
Indeed,
experiment
Caenorhabditis
elegans
significantly
increased
lifespan.
study
provides
new
insight
into
landscape
identifies
targets
interventions.
European Heart Journal,
Год журнала:
2024,
Номер
45(39), С. 4219 - 4235
Опубликована: Авг. 1, 2024
Vascular
smooth
muscle
cell
(VSMC)
senescence
is
crucial
for
the
development
of
atherosclerosis,
characterized
by
metabolic
abnormalities.
Tumour
necrosis
factor
receptor-associated
protein
1
(TRAP1),
a
regulator
associated
with
ageing,
might
be
implicated
in
atherosclerosis.
As
role
TRAP1
atherosclerosis
remains
elusive,
this
study
aimed
to
examine
function
VSMC
and
Frontiers in Physiology,
Год журнала:
2024,
Номер
15
Опубликована: Июль 2, 2024
Aging
is
a
complex
process
that
features
functional
decline
in
many
organelles.
Various
factors
influence
the
aging
process,
such
as
chromosomal
abnormalities,
epigenetic
changes,
telomere
shortening,
oxidative
stress,
and
mitochondrial
dysfunction.
Mitochondrial
dysfunction
significantly
impacts
because
mitochondria
regulate
cellular
energy,
balance,
calcium
levels.
integrity
maintained
by
mitophagy,
which
helps
maintain
homeostasis,
prevents
ROS
production,
protects
against
mtDNA
damage.
However,
increased
uptake
stress
can
disrupt
membrane
potential
permeability,
leading
to
apoptotic
cascade.
This
disruption
causes
production
of
free
radicals,
modification
accumulation
DNA
mutations,
contribute
aging.
dysfunction,
resulting
from
structural
linked
age-related
degenerative
diseases.
review
focuses
on
its
implications
disorders,
anti-aging
strategies
through
targeting
Annual Review of Physiology,
Год журнала:
2024,
Номер
86(1), С. 99 - 121
Опубликована: Фев. 12, 2024
The
elastic
properties
of
conductance
arteries
are
one
the
most
important
hemodynamic
functions
in
body,
and
data
continue
to
emerge
regarding
importance
their
dysfunction
vascular
aging
a
range
cardiovascular
diseases.
Here,
we
provide
new
insight
into
integrative
physiology
arterial
stiffening
its
clinical
consequence.
We
also
comprehensively
review
progress
made
on
pathways/molecules
that
appear
today
as
basic
determinants
stiffness,
particularly
those
mediating
smooth
muscle
cell
(VSMC)
contractility,
plasticity
stiffness.
focus
membrane
nuclear
mechanotransduction,
clearance
function
wall,
phenotypic
switching
VSMCs,
immunoinflammatory
stimuli
epigenetic
mechanisms.
Finally,
discuss
advances
latest
studies
revisit
classical
therapeutic
concepts
stiffness
lead
patient-by-patient
strategy
according
risk
exposure
underlying
disease.
Signal Transduction and Targeted Therapy,
Год журнала:
2025,
Номер
10(1)
Опубликована: Март 7, 2025
Redox
signaling
acts
as
a
critical
mediator
in
the
dynamic
interactions
between
organisms
and
their
external
environment,
profoundly
influencing
both
onset
progression
of
various
diseases.
Under
physiological
conditions,
oxidative
free
radicals
generated
by
mitochondrial
respiratory
chain,
endoplasmic
reticulum,
NADPH
oxidases
can
be
effectively
neutralized
NRF2-mediated
antioxidant
responses.
These
responses
elevate
synthesis
superoxide
dismutase
(SOD),
catalase,
well
key
molecules
like
nicotinamide
adenine
dinucleotide
phosphate
(NADPH)
glutathione
(GSH),
thereby
maintaining
cellular
redox
homeostasis.
Disruption
this
finely
tuned
equilibrium
is
closely
linked
to
pathogenesis
wide
range
Recent
advances
have
broadened
our
understanding
molecular
mechanisms
underpinning
dysregulation,
highlighting
pivotal
roles
genomic
instability,
epigenetic
modifications,
protein
degradation,
metabolic
reprogramming.
findings
provide
foundation
for
exploring
regulation
mechanistic
basis
improving
therapeutic
strategies.
While
antioxidant-based
therapies
shown
early
promise
conditions
where
stress
plays
primary
pathological
role,
efficacy
diseases
characterized
complex,
multifactorial
etiologies
remains
controversial.
A
deeper,
context-specific
signaling,
particularly
redox-sensitive
proteins,
designing
targeted
aimed
at
re-establishing
balance.
Emerging
small
molecule
inhibitors
that
target
specific
cysteine
residues
proteins
demonstrated
promising
preclinical
outcomes,
setting
stage
forthcoming
clinical
trials.
In
review,
we
summarize
current
intricate
relationship
disease
also
discuss
how
these
insights
leveraged
optimize
strategies
practice.
Frontiers in Immunology,
Год журнала:
2023,
Номер
14
Опубликована: Сен. 27, 2023
Post-acute
COVID-19
sequelae,
commonly
known
as
long
COVID,
encompasses
a
range
of
systemic
symptoms
experienced
by
significant
number
survivors.
The
underlying
pathophysiology
COVID
has
become
topic
intense
research
discussion.
While
chronic
inflammation
in
received
considerable
attention,
the
role
neutrophils,
which
are
most
abundant
all
immune
cells
and
primary
responders
to
inflammation,
been
unfortunately
overlooked,
perhaps
due
their
short
lifespan.
In
this
review,
we
discuss
emerging
neutrophil
extracellular
traps
(NETs)
persistent
inflammatory
response
observed
patients.
We
present
early
evidence
linking
persistence
NETs
pulmonary
fibrosis,
cardiovascular
abnormalities,
neurological
dysfunction
COVID.
Several
uncertainties
require
investigation
future
studies.
These
include
mechanisms
SARS-CoV-2
brings
about
sustained
activation
phenotypes
after
infection
resolution;
whether
heterogeneity
neutrophils
seen
acute
persists
into
phase;
presence
autoantibodies
can
induce
protect
them
from
degradation;
exert
differential,
organ-specific
effects;
specifically
NET
components
contribute
pathologies,
such
fibrosis;
senescent
drive
formation
through
pro-inflammatory
secretome
Answering
these
questions
may
pave
way
for
development
clinically
applicable
strategies
targeting
NETs,
providing
relief
health
crisis.
