Experimental and Therapeutic Medicine,
Journal Year:
2021,
Volume and Issue:
21(3)
Published: Jan. 18, 2021
The
mevalonate
(MVA)
pathway
serves
an
important
role
in
ventricular
remodeling.
Targeting
the
MVA
has
protective
effects
against
myocardial
fibrosis.
present
study
aimed
to
investigate
mechanism
behind
these
effects.
Primary
cultured
cardiac
fibroblasts
from
C57BL/6
mice
were
treated
in
vitro
5
groups:
i)
negative
control;
ii)
angiotensin
II
(Ang
II)
model
(1x10‑5
mol/l);
iii)
Ang
+
rosuvastatin
(ROS);
iv)
alendronate
(ALE);
and
v)
fasudil
(FAS).
Collagen
crystal
violet
staining
used
assess
morphological
changes
fibroblasts.
Reverse
transcription
quantitative
PCR
western
blotting
analyze
expression
of
key
signaling
molecules
involved
pathway.
ALE,
FAS,
ROS
groups
was
weak
compared
with
group,
while
rate
cell
proliferation
ROS,
FAS
slower
that
group.
In
addition,
pathway,
including
transforming
growth
factor‑β1
(TGF‑β1),
heat
shock
protein
47
(HSP47),
collagen
type
I
α1
(COL1A1),
vascular
endothelial
factor
2
(VEGF2)
fibroblast
(FGF2),
decreased
model.
Compared
3‑Hydroxy‑3‑Methylglutaryl‑CoA
reductase
(HMGCR)
gene
significantly
lowered
drug
intervention
groups,
whereas
farnesyl
pyrophosphate
synthase
(FDPS)
downregulated
ALE
but
elevated
groups.
ras
homolog
family
member
A
(RhoA)
whilst
kinase
reduced
Protein
TGF‑β1,
COL1A1
HSP47
following
each
three
drugs
Overall,
rosuvastatin,
aledronate
inhibited
synthesis.
Rosuvastatin
had
strongest
fibrosis
other
tested,
suggesting
this
be
a
potential
agent
for
clinical
treatment
cardiovascular
disease.
Diabetologia,
Journal Year:
2023,
Volume and Issue:
67(1), P. 19 - 26
Published: Nov. 30, 2023
Abstract
In
the
last
few
decades,
atherosclerotic
cardiovascular
disease
(ASCVD)
risk
has
decreased
dramatically
among
individuals
affected
by
familial
hypercholesterolaemia
(FH)
as
a
result
of
early
initiation
statin
treatment
in
childhood.
Contemporaneously
important
improvements
care
for
people
with
diabetes
have
also
been
made,
such
prevention
mortality
from
acute
diabetic
complications.
However,
type
1
still
two
to
eight
times
higher
death
than
general
population.
20
years,
landmark
studies
on
excess
diabetes,
particular
young
adults,
published.
Although
these
were
carried
out
different
populations,
all
reached
same
conclusion:
pronounced
increased
ASCVD.
this
review,
we
address
role
lipid
abnormalities
development
ASCVD
and
FH.
FH
are
diseases,
lessons
could
be
learned
statins
children
FH,
which
may
provide
rationale
more
stringent
control
dyslipidaemia
diabetes.
Graphical
Annals of Internal Medicine,
Journal Year:
2020,
Volume and Issue:
173(10), P. 806 - 812
Published: Sept. 21, 2020
Strategies
to
improve
patients'
tolerance
of
and
adherence
statins
may
enhance
the
effectiveness
dyslipidemia
treatment
in
those
at
risk
for
cardiovascular
disease
(CVD).To
assess
benefits
harms
interventions
statin
patients
CVD.MEDLINE,
EMBASE,
PubMed,
Cochrane
Library
from
December
2013
through
May
2019
(English
language
only).Systematic
reviews
(SRs),
randomized
controlled
trials
(RCTs),
cohort
studies
that
addressed
improving
adherence.One
investigator
abstracted
data
assessed
study
quality,
a
second
checked
abstractions
assessments
accuracy.One
SR,
1
RCT,
4
were
included.
The
SR
found
intensified
patient
care
improved
decreased
levels
total
serum
cholesterol
low-density
lipoprotein
(LDL-C)
6
months
or
more
follow-up.
Compared
with
discontinuation,
nondaily
dosing
lowered
LDL-C
levels.
One
large
suggested
than
90%
who
discontinued
could
be
rechallenged
same
different
adherent
year
after
statin-related
adverse
event
led
discontinuation.
Two
small
reported
previously
intolerant
had
low
baseline
vitamin
D
able
adhere
supplementation.This
is
qualitative
synthesis
new
evidence
existing
meta-analyses,
several
methodological
shortcomings.Although
strength
most
was
very
low,
rechallenge
(or
lower
dose)
seem
favorable
options
adherence.U.S.
Department
Veterans
Affairs.
Experimental and Therapeutic Medicine,
Journal Year:
2021,
Volume and Issue:
21(3)
Published: Jan. 18, 2021
The
mevalonate
(MVA)
pathway
serves
an
important
role
in
ventricular
remodeling.
Targeting
the
MVA
has
protective
effects
against
myocardial
fibrosis.
present
study
aimed
to
investigate
mechanism
behind
these
effects.
Primary
cultured
cardiac
fibroblasts
from
C57BL/6
mice
were
treated
in
vitro
5
groups:
i)
negative
control;
ii)
angiotensin
II
(Ang
II)
model
(1x10‑5
mol/l);
iii)
Ang
+
rosuvastatin
(ROS);
iv)
alendronate
(ALE);
and
v)
fasudil
(FAS).
Collagen
crystal
violet
staining
used
assess
morphological
changes
fibroblasts.
Reverse
transcription
quantitative
PCR
western
blotting
analyze
expression
of
key
signaling
molecules
involved
pathway.
ALE,
FAS,
ROS
groups
was
weak
compared
with
group,
while
rate
cell
proliferation
ROS,
FAS
slower
that
group.
In
addition,
pathway,
including
transforming
growth
factor‑β1
(TGF‑β1),
heat
shock
protein
47
(HSP47),
collagen
type
I
α1
(COL1A1),
vascular
endothelial
factor
2
(VEGF2)
fibroblast
(FGF2),
decreased
model.
Compared
3‑Hydroxy‑3‑Methylglutaryl‑CoA
reductase
(HMGCR)
gene
significantly
lowered
drug
intervention
groups,
whereas
farnesyl
pyrophosphate
synthase
(FDPS)
downregulated
ALE
but
elevated
groups.
ras
homolog
family
member
A
(RhoA)
whilst
kinase
reduced
Protein
TGF‑β1,
COL1A1
HSP47
following
each
three
drugs
Overall,
rosuvastatin,
aledronate
inhibited
synthesis.
Rosuvastatin
had
strongest
fibrosis
other
tested,
suggesting
this
be
a
potential
agent
for
clinical
treatment
cardiovascular
disease.