Ageing Research Reviews,
Journal Year:
2020,
Volume and Issue:
60, P. 101072 - 101072
Published: April 14, 2020
Cardiovascular
disease
(CVD)
is
the
most
common
to
increase
as
life
expectancy
increases.
Most
high-profile
pharmacological
treatments
for
age-related
CVD
have
led
inefficacious
results,
implying
that
novel
approaches
treating
these
pathologies
are
needed.
Emerging
data
demonstrated
senescent
cardiovascular
cells,
which
characterized
by
irreversible
cell
cycle
arrest
and
a
distinct
senescence-associated
secretory
phenotype,
accumulate
in
aged
or
diseased
systems,
suggesting
they
may
impair
function.
This
review
discusses
evidence
implicating
cells
ageing,
onset
progression
of
CVD,
molecular
mechanisms
underlying
senescence.
We
also
eradication
small-molecule-drug-mediated
apoptosis
immune
cell-mediated
efferocytosis
toxicity
promising
precisely
targeted
therapeutics
prevention
treatment.
International Journal of Molecular Sciences,
Journal Year:
2018,
Volume and Issue:
19(12), P. 3701 - 3701
Published: Nov. 22, 2018
Low-grade
chronic
inflammation
is
a
common
denominator
in
atherogenesis
and
related
diseases.
Solid
evidence
supports
the
occurrence
of
an
impairment
innate
adaptive
immune
system
with
senescence,
favoring
development
acute
age-related
Cardiovascular
(CV)
diseases
(CVD),
particular,
are
leading
cause
death
even
at
older
ages.
Inflammation-associated
mechanisms
that
contribute
to
CVD
include
dysregulated
redox
metabolic
pathways,
genetic
modifications,
infections/dysbiosis.
In
this
review,
we
will
recapitulate
determinants
consequences
dysfunction
age,
particular
focus
on
CV
system.
We
examine
currently
available
potential
future
strategies
counteract
accelerated
aging,
i.e.,
nutraceuticals,
probiotics,
caloric
restriction,
physical
activity,
smoking
alcohol
cessation,
control
low-grade
sources,
senolytic
senescence-modulating
drugs,
DNA-targeting
drugs.
Ageing Research Reviews,
Journal Year:
2020,
Volume and Issue:
60, P. 101072 - 101072
Published: April 14, 2020
Cardiovascular
disease
(CVD)
is
the
most
common
to
increase
as
life
expectancy
increases.
Most
high-profile
pharmacological
treatments
for
age-related
CVD
have
led
inefficacious
results,
implying
that
novel
approaches
treating
these
pathologies
are
needed.
Emerging
data
demonstrated
senescent
cardiovascular
cells,
which
characterized
by
irreversible
cell
cycle
arrest
and
a
distinct
senescence-associated
secretory
phenotype,
accumulate
in
aged
or
diseased
systems,
suggesting
they
may
impair
function.
This
review
discusses
evidence
implicating
cells
ageing,
onset
progression
of
CVD,
molecular
mechanisms
underlying
senescence.
We
also
eradication
small-molecule-drug-mediated
apoptosis
immune
cell-mediated
efferocytosis
toxicity
promising
precisely
targeted
therapeutics
prevention
treatment.