Cells,
Год журнала:
2023,
Номер
12(9), С. 1296 - 1296
Опубликована: Май 2, 2023
Senescent
cell
accumulation
has
been
observed
in
age-associated
diseases
including
cardiovascular
diseases.
cells
lack
proliferative
capacity
and
secrete
senescence-associated
secretory
phenotype
(SASP)
factors
that
may
cause
or
worsen
many
Therapies
targeting
senescent
cells,
especially
senolytic
drugs
selectively
induce
removal,
have
shown
to
delay,
prevent,
alleviate,
treat
multiple
preclinical
models.
Some
clinical
trials
already
completed
are
underway
for
a
number
of
geriatric
syndromes.
Understanding
how
cellular
senescence
affects
the
various
types
system,
such
as
endothelial
vascular
smooth
muscle
fibroblasts,
immune
progenitor
cardiomyocytes,
is
important
facilitate
translation
senotherapeutics
into
interventions.
This
review
highlights:
(1)
characteristics
their
involvement
diseases,
focusing
on
aforementioned
types,
(2)
evidence
about
other
senotherapeutics,
(3)
future
path
potential
Cells,
Год журнала:
2022,
Номер
11(3), С. 359 - 359
Опубликована: Янв. 21, 2022
Acute
inflammation
is
a
physiological
response
to
injury
or
infection,
with
cascade
of
steps
that
ultimately
lead
the
recruitment
immune
cells
clear
invading
pathogens
and
heal
wounds.
However,
chronic
arising
from
continued
presence
initial
trigger,
dysfunction
signalling
and/or
effector
pathways,
harmful
health.
While
successful
ageing
in
older
adults,
including
centenarians,
associated
low
levels
inflammation,
elevated
increases
risk
poor
health
death.
Hence
has
been
described
as
one
seven
pillars
ageing.
Age-associated
sterile,
chronic,
low-grade
commonly
termed
inflammageing-it
not
simply
consequence
increasing
chronological
age,
but
also
marker
biological
ageing,
multimorbidity,
mortality
risk.
inflammageing
was
initially
thought
be
caused
by
"continuous
antigenic
load
stress",
reports
last
two
decades
describe
much
more
complex
phenomenon
involving
cellular
senescence
system.
In
this
review,
we
explore
some
main
sources
consequences
context
immunosenescence
highlight
potential
interventions.
particular,
assess
contribution
age-associated
identify
patterns
pro-
anti-inflammatory
markers
characteristic
inflammageing,
alterations
system
finally
ways
diet,
exercise,
pharmacological
interventions
can
reduce
thus,
improve
later
life
With
aging,
there
is
increased
dysfunction
of
both
innate
and
adaptive
immune
responses,
which
contributes
to
impaired
responses
pathogens
greater
mortality
morbidity.
This
age-related
defined
in
general
as
immunosenescence
includes
an
increase
the
number
memory
T
cells,
loss
ability
respond
antigen
a
lingering
level
low-grade
inflammation.
However,
certain
features
are
similar
cellular
senescence,
irreversible
proliferation
response
damage
stress.
Importantly,
senescence
cells
can
develop
inflammatory
senescence-associated
secretory
phenotype
(SASP),
that
also
drives
non-autonomous
dysfunction.
Interestingly,
viral
infection
extent
directly
indirectly,
leading
inflammation,
especially
elderly.
review
focuses
on
dysfunction,
pathogens.
Cardiovascular Research,
Год журнала:
2022,
Номер
119(2), С. 336 - 356
Опубликована: Июль 25, 2022
Abstract
Long
COVID
has
become
a
world-wide,
non-communicable
epidemic,
caused
by
long-lasting
multiorgan
symptoms
that
endure
for
weeks
or
months
after
SARS-CoV-2
infection
already
subsided.
This
scientific
document
aims
to
provide
insight
into
the
possible
causes
and
therapeutic
options
available
cardiovascular
manifestations
of
long
COVID.
In
addition
chronic
fatigue,
which
is
common
symptom
COVID,
patients
may
present
with
chest
pain,
ECG
abnormalities,
postural
orthostatic
tachycardia,
newly
developed
supraventricular
ventricular
arrhythmias.
Imaging
heart
vessels
provided
evidence
chronic,
post-infectious
perimyocarditis
consequent
left
right
failure,
arterial
wall
inflammation,
microthrombosis
in
certain
patient
populations.
Better
understanding
underlying
cellular
molecular
mechanisms
will
aid
development
effective
treatment
strategies
its
manifestations.
A
number
have
been
proposed,
including
those
involving
direct
effects
on
myocardium,
microthrombotic
damage
endothelium,
persistent
inflammation.
Unfortunately,
existing
circulating
biomarkers,
coagulation,
inflammatory
markers,
are
not
highly
predictive
either
presence
outcome
when
measured
3
infection.
Further
studies
needed
understand
mechanisms,
identify
specific
guide
future
preventive
treatments
address
sequelae.
Science Translational Medicine,
Год журнала:
2022,
Номер
14(664)
Опубликована: Июль 7, 2022
A
subset
of
individuals
who
recover
from
coronavirus
disease
2019
(COVID-19)
develop
post-acute
sequelae
severe
acute
respiratory
syndrome
2
(SARS-CoV-2)
(PASC),
but
the
mechanistic
basis
PASC-associated
lung
abnormalities
suffers
a
lack
longitudinal
tissue
samples.
The
mouse-adapted
SARS-CoV-2
strain
MA10
produces
an
distress
in
mice
similar
to
humans.
To
investigate
PASC
pathogenesis,
studies
MA10-infected
were
extended
clinical
recovery
phases.
At
15
120
days
after
virus
clearance,
pulmonary
histologic
findings
included
subpleural
lesions
composed
collagen,
proliferative
fibroblasts,
and
chronic
inflammation,
including
tertiary
lymphoid
structures.
Longitudinal
spatial
transcriptional
profiling
identified
global
reparative
fibrotic
pathways
dysregulated
diseased
regions,
human
COVID-19.
Populations
alveolar
intermediate
cells,
coupled
with
focal
up-regulation
profibrotic
markers,
persistently
regions.
Early
intervention
antiviral
EIDD-2801
reduced
disease,
early
antifibrotic
agent
(nintedanib)
modified
severity.
This
murine
model
provides
opportunities
identify
associated
persistent
test
countermeasures
ameliorate
PASC.
The Lancet Healthy Longevity,
Год журнала:
2022,
Номер
3(1), С. e67 - e77
Опубликована: Янв. 1, 2022
Cellular
senescence
is
a
major
contributor
to
age-related
diseases
in
humans;
however,
it
also
has
beneficial
role
physiological
and
pathological
processes,
including
wound
healing,
host
immunity,
tumour
suppression.
Reducing
the
burden
of
cell
animal
models
cardiometabolic
disorders,
inflammatory
conditions,
neurodegenerative
diseases,
cancer
using
pharmaceutical
approaches
that
selectively
target
senescent
cells
(ie,
senolytics)
or
suppress
senescence-associated
secretory
phenotype
senomorphics)
holds
great
promise
for
management
chronic
age-associated
conditions.
Although
studies
have
provided
evidence
senolytics
senomorphics
are
effective
at
decreasing
number
humans,
short-term
long-term
side-effects
these
therapies
largely
unknown.
In
this
Review,
we
systematically
discuss
been
investigated
clinical
trials
used
off-label,
presenting
their
various
adverse
effects.
Despite
potential
senotherapeutics
transform
anti-ageing
medicine,
cautionary
approach
regarding
unwanted
dose-dependent
should
be
adopted.
Frontiers in Cell and Developmental Biology,
Год журнала:
2022,
Номер
10
Опубликована: Фев. 16, 2022
Cellular
senescence
is
a
process
that
leads
to
state
of
irreversible
cell
growth
arrest
induced
by
variety
intrinsic
and
extrinsic
stresses.
Senescent
cells
(SnCs)
accumulate
with
age
have
been
implicated
in
various
age-related
diseases
part
via
expressing
the
senescence-associated
secretory
phenotype.
Elimination
SnCs
has
potential
delay
aging,
treat
extend
healthspan.
However,
once
becoming
senescent,
they
are
more
resistant
apoptotic
stimuli.
Senolytics
can
selectively
eliminate
targeting
SnC
anti-apoptotic
pathways
(SCAPs).
They
developed
as
novel
pharmacological
strategy
diseases.
heterogeneity
indicates
depend
on
different
proteins
or
for
their
survival.
Thus,
better
understanding
underlying
mechanisms
resistance
will
provide
new
molecular
targets
development
cell-specific
broad-spectrum
therapeutics
clear
SnCs.
In
this
review,
we
discussed
latest
research
progresses
challenge
senolytic
development,
described
significance
regulation
apoptosis
systematically
summarized
SCAPs
involved
International Journal of Molecular Sciences,
Год журнала:
2022,
Номер
23(4), С. 2176 - 2176
Опубликована: Фев. 16, 2022
The
aging
of
mammals
is
accompanied
by
the
progressive
atrophy
tissues
and
organs
accumulation
random
damage
to
macromolecular
DNA,
protein,
lipids.
Flavonoids
have
excellent
antioxidant,
anti-inflammatory,
neuroprotective
effects.
Recent
studies
shown
that
flavonoids
can
delay
prolong
a
healthy
lifespan
eliminating
senescent
cells,
inhibiting
senescence-related
secretion
phenotypes
(SASPs),
maintaining
metabolic
homeostasis.
However,
only
few
systematic
described
in
clinical
treatment
for
anti-aging,
which
needs
be
explored
further.
This
review
first
highlights
association
between
damage.
Then,
we
discuss
advances
role
flavonoid
molecules
prolonging
health
span
organisms.
study
may
provide
crucial
information
drug
design
developmental
applications
based
on
flavonoids.
