The Journal of Cardiovascular Aging,
Год журнала:
2024,
Номер
4(4)
Опубликована: Ноя. 19, 2024
Cardiovascular
diseases
(CVDs)
and
cancer
are
the
two
leading
causes
of
global
mortality.
Cancer
treatments,
including
radiotherapy
chemotherapy,
can
have
severe
cardiotoxic
side
effects,
raising
concerns
for
patients
increasing
financial
burden
on
healthcare
systems.
Recent
studies
shown
a
link
between
therapy-induced
cardiotoxicity
cardiac
senescence.
Specifically,
systemic
therapies
known
to
induce
senescence,
which
may
directly
result
in
dysfunction
or
enhance
vulnerability
heart
other
stressors.
Besides
anthracyclines,
newer,
more
targeted
such
as
tyrosine
kinase
inhibitors
(TKIs)
also
been
Cellular
senescence
is
triggered
by
DNA
damage,
oncogene
activation,
reactive
oxygen
nitrogen
species,
stressors,
secretion
proinflammatory
factors,
increased
oxidative
stress,
disruption
normal
cellular
functions.
Understanding
molecular
mechanisms
induced
therapy
essential
attenuating
even
preventing
clinically
overt
using
senotherapies
senolytics
senomorphics.
In
this
review,
that
associated
with
CVDs
described
an
emphasis
potential
role
disease
progression.
addition,
particularly
doxorubicin
(DOX),
radiotherapy,
TKIs
lead
highlighted.
Finally,
recent
novel
treating
discussed
focus
targeting
following
treatment.
The
field
remains
its
early
stages,
further
research
required
clarify
how
treatments
contribute
cardiotoxicity.
At
same
time,
identifying
be
safely
combined
drugs
protecting
health
patients.
The American Journal of Sports Medicine,
Год журнала:
2024,
Номер
52(14), С. 3625 - 3640
Опубликована: Ноя. 3, 2024
Background:
Microfracture
is
one
surgical
treatment
strategy
for
osteochondral
lesions
of
the
talus
(OLTs)
but
results
in
fibrocartilage
repair
tissue,
which
has
inferior
mechanical
properties
to
native
hyaline
cartilage.
Biological
regulation
microfracture
been
suggested
improve
quality
cartilage
patients.
Purpose:
To
determine
if
administration
losartan,
fisetin,
or
losartan
and
fisetin
combined
can
enhance
microfracture-mediated
OLTs
a
rabbit
model.
Study
Design:
Controlled
laboratory
study.
Methods:
Four-month-old
female
rabbits
were
divided
into
following
groups
(8
per
group):
only
(microfracture),
plus
(losartan),
(fisetin),
(losartan+fisetin).
A
2.7-mm
defect
4
holes
created
talar
dome
The
administered
(10
mg/kg/day),
(20
orally
until
euthanized
12
weeks
after
surgery.
Gross
evaluation,
micro–computed
tomography,
histology,
immunohistochemistry
evaluations
defects
performed
as
well
quantitative
polymerase
chain
reaction
capsule
tissue
enzyme-linked
immunosorbent
assay
serum.
Results:
had
increased
International
Cartilage
Regeneration
&
Joint
Preservation
Society
macroscopic
scores
with
improved
enhanced
subchondral
bone
healing
compared
group.
However,
losartan+fisetin
group
did
not
show
synergistic
effect.
O’Driscoll
histology
higher
group,
while
lower
score
than
groups.
Collagen
type
2
staining
revealed
organized
chondrocytes
groups,
improvement
when
other
Fisetin
decreased
catalase
transforming
growth
factor-β1–activated
kinase
1
expression
capsular
tissue.
Conclusion:
Concomitant
biological
regulation,
using
oral
either
may
OLTs;
however,
current
drug
regimen
does
appear
provide
effects.
Clinical
Relevance:
Oral
intake
result
beneficial
effects
on
OLTs.
The Journal of Cardiovascular Aging,
Год журнала:
2024,
Номер
4(4)
Опубликована: Ноя. 19, 2024
Cardiovascular
diseases
(CVDs)
and
cancer
are
the
two
leading
causes
of
global
mortality.
Cancer
treatments,
including
radiotherapy
chemotherapy,
can
have
severe
cardiotoxic
side
effects,
raising
concerns
for
patients
increasing
financial
burden
on
healthcare
systems.
Recent
studies
shown
a
link
between
therapy-induced
cardiotoxicity
cardiac
senescence.
Specifically,
systemic
therapies
known
to
induce
senescence,
which
may
directly
result
in
dysfunction
or
enhance
vulnerability
heart
other
stressors.
Besides
anthracyclines,
newer,
more
targeted
such
as
tyrosine
kinase
inhibitors
(TKIs)
also
been
Cellular
senescence
is
triggered
by
DNA
damage,
oncogene
activation,
reactive
oxygen
nitrogen
species,
stressors,
secretion
proinflammatory
factors,
increased
oxidative
stress,
disruption
normal
cellular
functions.
Understanding
molecular
mechanisms
induced
therapy
essential
attenuating
even
preventing
clinically
overt
using
senotherapies
senolytics
senomorphics.
In
this
review,
that
associated
with
CVDs
described
an
emphasis
potential
role
disease
progression.
addition,
particularly
doxorubicin
(DOX),
radiotherapy,
TKIs
lead
highlighted.
Finally,
recent
novel
treating
discussed
focus
targeting
following
treatment.
The
field
remains
its
early
stages,
further
research
required
clarify
how
treatments
contribute
cardiotoxicity.
At
same
time,
identifying
be
safely
combined
drugs
protecting
health
patients.
