Cells,
Год журнала:
2022,
Номер
11(7), С. 1249 - 1249
Опубликована: Апрель 6, 2022
Cardiac
hypertrophy,
initiated
by
a
variety
of
physiological
or
pathological
stimuli
(hemodynamic
hormonal
stimulation
infarction),
is
critical
early
adaptive
compensatory
response
the
heart.
The
structural
basis
progression
from
compensated
hypertrophy
to
and
heart
failure
still
largely
unknown.
In
most
cases,
activation
an
inflammatory
program
reflects
reparative
protective
other
primary
injurious
processes.
Later
on,
regardless
underlying
etiology,
always
associated
with
both
local
systemic
signaling
cascades.
macrophages
are
nodal
regulators
inflammation.
Resident
mostly
attenuate
cardiac
injury
secreting
cytoprotective
factors
(cytokines,
chemokines,
growth
factors),
scavenging
damaged
cells
mitochondrial
debris,
regulating
conduction,
angiogenesis,
lymphangiogenesis,
fibrosis.
contrast,
excessive
recruitment
monocyte-derived
contributes
transition
failure.
current
review
examines
ambivalent
role
inflammation
(mainly
TNFα-related)
(Mφ)
in
pathophysiologies
non-infarction
origin,
focusing
on
Our
objective
illustrate
how
harnessing
this
knowledge
could
pave
way
for
innovative
therapeutics
patients
Signal Transduction and Targeted Therapy,
Год журнала:
2022,
Номер
7(1)
Опубликована: Дек. 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.
Abstract
Cardiovascular
disease
is
the
leading
cause
of
death
in
individuals
over
60
years
old.
Aging
associated
with
an
increased
prevalence
coronary
artery
and
a
poorer
prognosis
following
acute
myocardial
infarction
(MI).
With
age,
senescent
cells
accumulate
tissues,
including
heart,
contribute
to
age‐related
pathologies.
However,
role
senescence
recovery
MI
has
not
been
investigated.
In
this
study,
we
demonstrate
that
treatment
aged
mice
senolytic
drug,
navitoclax,
eliminates
cardiomyocytes
attenuates
profibrotic
protein
expression
mice.
Importantly,
clearance
improved
remodelling
diastolic
function
as
well
overall
survival
MI.
These
data
provide
proof‐of‐concept
evidence
are
major
contributors
impaired
mortality
senolytics
potential
new
therapeutic
avenue
for
Cardiovascular Research,
Год журнала:
2021,
Номер
118(5), С. 1173 - 1187
Опубликована: Май 5, 2021
Abstract
Cellular
senescence
is
a
state
of
irreversible
cell
cycle
arrest
associated
with
ageing.
Senescence
different
cardiac
types
can
direct
the
pathophysiology
cardiovascular
diseases
(CVDs)
such
as
atherosclerosis,
myocardial
infarction,
and
fibrosis.
While
age-related
telomere
shortening
represents
major
cause
replicative
senescence,
senescent
also
be
induced
by
oxidative
stress,
metabolic
dysfunction,
epigenetic
regulation,
among
other
stressors.
It
critical
that
we
understand
molecular
pathways
lead
to
cellular
consequences
in
order
develop
new
therapeutic
approaches
treat
CVD.
In
this
review,
discuss
mechanisms
explore
how
(including
cardiomyocytes,
endothelial
cells,
fibroblasts,
vascular
smooth
muscle
valve
interstitial
cells)
CVD,
highlight
potential
target
prevent
or
Aging and Disease,
Год журнала:
2022,
Номер
13(1), С. 103 - 103
Опубликована: Янв. 1, 2022
Aging
is
a
prominent
risk
factor
for
cardiovascular
diseases,
which
the
leading
cause
of
death
around
world.
Recently,
cellular
senescence
has
received
potential
attention
as
promising
target
in
preventing
including
acute
myocardial
infarction,
atherosclerosis,
cardiac
aging,
pressure
overload-induced
hypertrophy,
heart
regeneration,
hypertension,
and
abdominal
aortic
aneurysm.
Here,
we
discuss
mechanisms
underlying
describe
involvement
senescent
cells
(including
cardiomyocytes,
endothelial
cells,
vascular
smooth
muscle
fibroblasts/myofibroblasts
T
cells)
age-related
diseases.
Then,
highlight
targets
(SIRT1
mTOR)
that
regulating
disorders.
Furthermore,
review
evidence
can
exert
both
beneficial
detrimental
implications
diseases
on
context-dependent
manner.
Finally,
summarize
emerging
pro-senescent
or
anti-senescent
interventions
their
therapeutic
Abstract
The
population
of
cancer
survivors
is
rapidly
increasing
due
to
improving
healthcare.
However,
therapies
often
have
long-term
side
effects.
One
example
therapy-related
cardiac
dysfunction
(CTRCD)
caused
by
doxorubicin:
up
9%
the
patients
treated
with
this
drug
develop
heart
failure
at
a
later
stage.
In
recent
years,
doxorubicin-induced
cardiotoxicity
has
been
associated
an
accelerated
aging
phenotype
and
cellular
senescence
in
heart.
review
we
explain
evidence
doxorubicin-treated
comparing
it
healthy
aged
hearts,
shed
light
on
treatment
strategies
that
are
proposed
pre-clinical
settings.
We
will
discuss
impact
could
clinic
future
research.
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
Experimental Gerontology,
Год журнала:
2024,
Номер
188, С. 112389 - 112389
Опубликована: Март 8, 2024
Aging-related
diseases
(ARDs)
are
a
major
global
health
concern,
and
the
development
of
effective
therapies
is
urgently
needed.
Kaempferol,
flavonoid
found
in
several
plants,
has
emerged
as
promising
candidate
for
ameliorating
ARDs.
This
comprehensive
review
examines
Kaempferol's
chemical
properties,
safety
profile,
pharmacokinetics,
highlights
its
potential
therapeutic
utility
against
underpinned
by
distinctive
structure,
which
confers
antioxidative
anti-inflammatory
properties.
Kaempferol
counteracts
reactive
oxygen
species
(ROS)
modulates
crucial
cellular
pathways,
thereby
combating
oxidative
stress
inflammation,
hallmarks
low
toxicity
wide
margins,
demonstrated
preclinical
clinical
studies,
further
substantiate
potential.
Compelling
evidence
supports
substantial
addressing
ARDs
through
mechanisms,
notably
anti-inflammatory,
antioxidant,
anti-apoptotic
actions.
exhibits
versatile
neuroprotective
effect
modulating
various
proinflammatory
signaling
including
NF-kB,
p38MAPK,
AKT,
β-catenin
cascade.
Additionally,
it
hinders
formation
aggregation
beta-amyloid
protein
regulates
brain-derived
neurotrophic
factors.
In
terms
anticancer
potential,
kaempferol
acts
diverse
inducing
apoptosis,
arresting
cell
cycle
at
G2/M
phase,
suppressing
epithelial-mesenchymal
transition
(EMT)-related
markers,
affecting
phosphoinositide
3-kinase/protein
kinase
B
pathways.
Subsequent
studies
should
focus
on
refining
dosage
regimens,
exploring
innovative
delivery
systems,
conducting
trials
to
translate
these
findings
into
applications.
Cell Death Discovery,
Год журнала:
2024,
Номер
10(1)
Опубликована: Фев. 14, 2024
Abstract
Cardiac
aging,
particularly
cardiac
cell
senescence,
is
a
natural
process
that
occurs
as
we
age.
Heart
function
gradually
declines
in
old
age,
leading
to
continuous
heart
failure,
even
people
without
prior
history
of
disease.
To
address
this
issue
and
improve
function,
it
crucial
investigate
the
molecular
mechanisms
underlying
senescence.
This
review
summarizes
main
key
proteins
involved
further
discusses
modulators
cellular
senescence
aging
hearts.
Furthermore,
discussion
will
encompass
comprehensive
descriptions
drugs,
modes
action
potential
targets
for
intervention
By
offering
fresh
perspective
insights
into
seeks
provide
important
theoretical
foundations
development
drugs
targeting
condition.
