Frontiers in Cardiovascular Medicine,
Год журнала:
2021,
Номер
8
Опубликована: Ноя. 12, 2021
Cardiovascular
diseases
(CVDs)
represent
a
major
global
health
problem,
due
to
their
continued
high
incidences
and
mortality.
The
last
few
decades
have
witnessed
new
advances
in
clinical
research
which
led
increased
survival
recovery
CVD
patients.
Nevertheless,
elusive
multifactorial
pathophysiological
mechanisms
of
development
perplexed
researchers
identifying
efficacious
therapeutic
interventions.
Search
for
novel
effective
strategies
diagnosis,
prevention,
intervention
has
shifted
focus
on
extracellular
vesicles
(EVs)
recent
years.
By
transporting
molecular
cargo
from
donor
recipient
cells,
EVs
modulate
gene
expression
influence
the
phenotype
thus
prove
be
an
imperative
component
intercellular
signaling.
Elucidation
role
communications
under
physiological
conditions
implied
enormous
potential
monitoring
treatment
CVD.
secreted
myriad
cells
cardiovascular
system
such
as
cardiomyocytes,
cardiac
fibroblasts,
progenitor
endothelial
inflammatory
may
facilitate
communication
pathological
conditions.
Understanding
EVs-mediated
cellular
delineate
mechanism
origin
progression
diseases.
current
review
summarizes
exosome-mediated
paracrine
signaling
leading
disease.
mechanistic
exosomes
disease
will
provide
avenues
designing
diagnosis
World Journal of Diabetes,
Год журнала:
2010,
Номер
1(2), С. 36 - 36
Опубликована: Янв. 1, 2010
Insulin
resistance
is
a
hallmark
of
obesity,
diabetes,
and
cardiovascular
diseases,
leads
to
many
the
abnormalities
associated
with
metabolic
syndrome.Our
understanding
insulin
has
improved
tremendously
over
years,
but
certain
aspects
its
estimation
still
remain
elusive
researchers
clinicians.The
quantitative
assessment
sensitivity
not
routinely
used
during
biochemical
investigations
for
diagnostic
purposes,
em
erging
importance
led
wider
application
research
studies.Evaluation
number
clinical
states
where
compromised
calls
resistance.Insulin
increasingly
being
assessed
in
various
disease
conditions
it
aids
examining
their
pathogenesis,
etiology
consequences.The
hyperinsulinemic
euglycemic
glucose
clamp
gold
standard
method
determination
sensitivity,
impractical
as
labor
timeintensive.A
surrogate
indices
have
therefore
been
employed
simplify
improve
resistance.The
object
this
review
highlight
methodologies
current
upcoming
measures
sensitivity/resistance.Indepth
knowledge
these
markers
will
help
better
exploitation
condition.
Experimental & Molecular Medicine,
Год журнала:
2014,
Номер
46(6), С. e99 - e99
Опубликована: Июнь 6, 2014
CD36
is
a
membrane
glycoprotein
that
present
on
various
types
of
cells,
including
monocytes,
macrophages,
microvascular
endothelial
adipocytes
and
platelets.
Macrophage
participates
in
atherosclerotic
arterial
lesion
formation
through
its
interaction
with
oxidized
low-density
lipoprotein
(oxLDL),
which
triggers
signaling
cascades
for
inflammatory
responses.
functions
oxLDL
uptake
foam
cell
formation,
the
initial
critical
stage
atherosclerosis.
In
addition,
via
inhibits
macrophage
migration,
may
be
macrophage-trapping
mechanism
lesions.
The
role
was
examined
vitro
studies
vivo
experiments,
investigated
atherosclerosis
revealed
deficiency
reduces
formation.
Platelet
also
promotes
processes
involved
thrombus
after
plaque
rupture.
Because
an
essential
component
atherosclerosis,
defining
function
corresponding
pathway
lead
to
new
treatment
strategy
CD36,
protein
found
surface
immune
cells
blood
vessel
key
Young
Mi
Park
from
Ewha
Womans
University
School
Medicine
Seoul,
South
Korea,
reviews
how
macrophages
binds
form
‘bad’
cholesterol
called
lipoprotein.
This
binding
series
reactions
leads
inflammation
fat-laden
plaque-build
up
inner
lining
vessels.
platelets
responses
clots
plaques
argues
better
understanding
could
treatments
condition
commonly
associated
increased
risk
heart
attack
stroke.
Journal of Cellular and Molecular Medicine,
Год журнала:
2015,
Номер
20(1), С. 17 - 28
Опубликована: Окт. 23, 2015
Abstract
Formation
of
foam
cells
is
a
hallmark
at
the
initial
stages
atherosclerosis.
Monocytes
attracted
by
pro‐inflammatory
stimuli
attach
to
inflamed
vascular
endothelium
and
penetrate
arterial
intima
where
they
differentiate
macrophages.
Intimal
macrophages
phagocytize
oxidized
low‐density
lipoproteins
(ox
LDL
).
Several
scavenger
receptors
(
SR
),
including
CD
36,
‐A1
lectin‐like
ox
receptor‐1
LOX
‐1),
mediate
uptake.
In
late
endosomes/lysosomes
macrophages,
are
catabolysed.
Lysosomal
acid
lipase
LAL
)
hydrolyses
cholesterol
esters
that
enriched
in
free
fatty
acids.
endoplasmic
reticulum
ER
acyl
coenzyme
A:
acyltransferase‐1
ACAT
1)
turn
catalyses
esterification
store
as
lipid
droplets
Neutral
cholesteryl
ester
hydrolases
nCEH
NCEH
1
involved
secondary
hydrolysis
liberate
could
be
then
out‐flowed
from
ATP
‐binding
cassette
ABC
transporters
ABCA
ABCG
‐
BI
.
atherosclerosis,
disruption
homoeostasis
leads
accumulation
formation
cells.
Cell Death and Disease,
Год журнала:
2020,
Номер
11(9)
Опубликована: Сен. 25, 2020
Abstract
Non-alcoholic
fatty
liver
disease
(NAFLD)
is
the
most
common
cause
of
chronic
worldwide.
NAFLD
stages
range
from
simple
steatosis
(NAFL)
to
non-alcoholic
steatohepatitis
(NASH)
which
can
progress
cirrhosis
and
hepatocellular
carcinoma.
One
crucial
events
clearly
involved
in
progression
lipotoxicity
resulting
an
excessive
acid
(FFA)
influx
hepatocytes.
Hepatic
occurs
when
capacity
hepatocyte
manage
export
FFAs
as
triglycerides
(TGs)
overwhelmed.
This
review
provides
succinct
insights
into
molecular
mechanisms
responsible
for
NAFLD,
including
ER
oxidative
stress,
autophagy,
lipoapotosis
inflammation.
In
addition,
we
highlight
role
CD36/FAT
translocase
pathogenesis.
Up-to-date,
it
well
known
that
CD36
increases
FFA
uptake
and,
liver,
drives
hepatosteatosis
onset
might
contribute
its
NASH.
Clinical
studies
have
reinforced
significance
by
showing
increased
content
patients.
Interestingly,
circulating
levels
a
soluble
form
(sCD36)
are
abnormally
elevated
patients
positively
correlate
with
histological
grade
hepatic
steatosis.
fact,
induction
translocation
plasma
membrane
hepatocytes
may
be
determining
factor
physiopathology
Given
all
these
data,
targeting
or
some
functional
regulators
promising
therapeutic
approach
prevention
treatment
NAFLD.
Cardiovascular Research,
Год журнала:
2007,
Номер
75(3), С. 468 - 477
Опубликована: Март 15, 2007
CD36
is
a
multi-ligand
scavenger
receptor
present
on
the
surface
of
number
cells
such
as
platelets,
monocytes/macrophages,
endothelial
and
smooth
muscle
cells.
Monocyte/macrophage
has
been
shown
to
play
critical
role
in
development
atherosclerotic
lesions
by
its
capacity
bind
endocytose
oxidized
low
density
lipoproteins
(OxLDL),
it
implicated
formation
foam
However,
significance
atherosclerosis
recently
called
into
question
different
studies,
therefore
exact
still
needs
be
clarified.
The
aim
this
article
carefully
review
importance
an
essential
component
pathogenesis
atherosclerosis.
The Journal of Experimental Medicine,
Год журнала:
2022,
Номер
219(6)
Опубликована: Апрель 19, 2022
CD36
is
a
type
2
cell
surface
scavenger
receptor
widely
expressed
in
many
immune
and
non-immune
cells.
It
functions
as
both
signaling
responding
to
DAMPs
PAMPs,
well
long
chain
free
fatty
acid
transporter.
Recent
studies
have
indicated
that
can
integrate
metabolic
pathways
through
its
dual
thereby
influence
differentiation
activation,
ultimately
help
determine
fate.
Its
expression
along
with
innate
adaptive
cells
contribute
pathogenesis
of
common
diseases,
including
atherosclerosis
tumor
progression,
which
makes
downstream
effectors
potential
therapeutic
targets.
This
review
comprehensively
examines
the
variety
cells,
especially
macrophages
T
We
also
briefly
discuss
function
such
adipocytes
platelets,
impact
system
via
intercellular
communication.
Finally,
outstanding
questions
this
field
are
provided
for
directions
future
studies.
Journal of Diabetes Science and Technology,
Год журнала:
2010,
Номер
4(3), С. 685 - 693
Опубликована: Май 1, 2010
Metabolic
syndrome
is
associated
with
insulin
resistance,
elevated
glucose
and
lipids,
inflammation,
decreased
antioxidant
activity,
increased
weight
gain,
glycation
of
proteins.
Cinnamon
has
been
shown
to
improve
all
these
variables
in
vitro,
animal,
and/or
human
studies.
In
addition,
cinnamon
alleviate
factors
Alzheimer's
disease
by
blocking
reversing
tau
formation
vitro
ischemic
stroke
cell
swelling.
studies
also
show
that
components
control
angiogenesis
the
proliferation
cancer
cells.
Human
involving
subjects
metabolic
syndrome,
type
2
diabetes
mellitus,
polycystic
ovary
beneficial
effects
whole
aqueous
extracts
on
glucose,
insulin,
sensitivity,
status,
blood
pressure,
lean
body
mass,
gastric
emptying.
However,
not
have
positive
cinnamon,
amount
as
well
drugs
are
taking,
likely
affect
response
cinnamon.
summary,
may
be
important
alleviation
prevention
signs
symptoms
diabetes,
cardiovascular
related
diseases.
Gynecological Endocrinology,
Год журнала:
2010,
Номер
26(4), С. 281 - 296
Опубликована: Фев. 8, 2010
Hirsutism
is
a
common
endocrine
disorder,
defined
as
increased
growth
of
terminal
hairs
in
male
pattern.
most
often
caused
by
polycystic
ovary
syndrome
(PCOS),
whereas
only
5%
patients
are
diagnosed
with
rare
diseases.
PCOS
may
be
considered
multiorgan
disease
causing
not
adrenal
and
ovarian
sex
hormone
secretion
but
also
changed
gonadotrophins,
hormone,
adrenocorticotrophic
(ACTH)
from
the
pituitary.
The
majority
insulin
resistant
characterized
an
inflammatory
state
abdominal
obesity
interleukins,
chemokines,
adipokines.
therefore
associated
risk
metabolic
type
2
diabetes
(T2D).
Patients
hirsutism
present
bone
mineral
density
despite
decreased
D-vitamin
levels.
etiology
to
likely
multifactorial
including
both
genetic
environmental
factors
such
fetal
stress
intrauterine
retardation.
In
review,
we
give
comprehensive
overview
pathophysiology
multiple
disturbances
PCOS.
Human Molecular Genetics,
Год журнала:
2010,
Номер
20(1), С. 193 - 201
Опубликована: Окт. 8, 2010
Membrane
CD36
functions
in
the
uptake
of
fatty
acids
(FAs),
oxidized
lipoproteins
and
signal
transduction
after
binding
these
ligands.
In
rodents,
is
implicated
abnormal
lipid
metabolism,
inflammation
atherosclerosis.
humans,
variants
have
been
identified
to
influence
free
FA
high-density
lipoprotein
(HDL)
levels
associate
with
risk
metabolic
syndrome,
coronary
artery
disease
stroke.
this
study,
15
common
lipid-associated
single
nucleotide
polymorphisms
(SNPs)
were
evaluated
for
impact
on
monocyte
expression
(protein
transcript)
104
African
Americans.
a
subset
subjects,
SNPs
tested
association
surface
(n
=
65)
platelet
total
57).
The
relationship
between
serum
HDL
very
low-density
(VLDLs)
was
also
examined.
After
permutation-based
correction
multiple
tests,
four
(rs1761667,
rs3211909,
rs3211913,
rs3211938)
influenced
protein
two
(rs3211909,
CD36.
effect
HDL-associated
inversely
related
potential
causality
supported
by
Mendelian
randomization
analysis.
Consistent
this,
negatively
correlated
subfractions.
contrast,
positive
correlations
documented
VLDL
lipid,
particle
number
apolipoprotein
B.
conclusion,
that
reduce
appear
promote
protective
profile.
study
may
predictive
susceptibility
Further
studies
are
warranted
validate
determine
whether
findings
population
specific.