Diabetes Metabolic Syndrome and Obesity,
Год журнала:
2019,
Номер
Volume 12, С. 1297 - 1309
Опубликована: Авг. 1, 2019
Diabetic
nephropathy
(DN)
is
a
lethal
diabetic
microvascular
complication
characterized
by
chronic
low-grade
inflammation.
The
NOD-like
receptor
pyrin
domain-containing
protein
3
(NLRP3)
inflammasome
implicated
in
the
progression
of
DN.
MCC950
selective
and
potent
inhibitor
NLRP3;
however,
its
efficacy
DN
requires
further
investigation.
To
investigate
DN,
eight-week-old
type
2
db/db
mice
received
injections
intraperitoneally
(10
mg/kg)
twice
per
week
for
12
weeks.
Urinary
albumin-to-creatinine
ratio
(ACR)
neutrophil
gelatinase-associated
lipocalin
(NGAL),
renal
function,
pathological
changes,
markers
podocyte
fibrosis
NLPR3/caspase-1/IL-1β
expression
cortices
were
evaluated.
High-glucose
(HG)-treated
rat
glomerular
mesangial
cells
treated
with
various
concentrations
48
hrs.
Markers
measured.
NLRP3
was
activated
HG-induced
upregulating
NLRP3/caspase-1/IL-1β
pathway.
Inhibition
reduced
production
active
caspase-1
IL-1β
cells.
serum
creatinine,
urinary
ACR
NGAL,
attenuated
expansion
increased
matrix
tubular
dilatation,
alleviated
thickened
basement
membrane
(GBM)
foot
process
fusion
without
affecting
body
weight
blood
glucose
levels
mice.
podocin
mice,
decreased
TGF-β1,
fibronectin,
collagen
I
α-smooth
muscle
actin
(α-SMA)
ameliorated
GBM,
injury
effectively
kidney
inhibiting
pathway,
which
may
be
potential
therapeutic
strategy
to
prevent
Journal of the Formosan Medical Association,
Год журнала:
2018,
Номер
117(8), С. 662 - 675
Опубликована: Март 2, 2018
Diabetic
kidney
disease
(DKD)
is
a
major
cause
of
morbidity
and
mortality
in
patients
with
diabetes
mellitus
the
leading
end-stage
renal
world.
The
most
characteristic
marker
DKD
albuminuria,
which
associated
progression
cardiovascular
events.
Renal
hemodynamics
changes,
oxidative
stress,
inflammation,
hypoxia
overactive
renin-angiotensin-aldosterone
system
(RAAS)
are
involved
pathogenesis
DKD,
fibrosis
plays
key
role.
Intensified
multifactorial
interventions,
including
RAAS
blockades,
blood
pressure
glucose
control,
quitting
smoking,
help
to
prevent
development
progression.
In
recent
years,
novel
agents
applied
for
preventing
progression,
new
types
glucose-lowering
agents,
pentoxifylline,
vitamin
D
analog
paricalcitol,
pyridoxamine,
ruboxistaurin,
soludexide,
Janus
kinase
inhibitors
nonsteroidal
minerocorticoid
receptor
antagonists.
this
review,
large
studies
about
also
summarized.
International Journal of Molecular Sciences,
Год журнала:
2019,
Номер
20(3), С. 649 - 649
Опубликована: Фев. 2, 2019
Interleukin
(IL)-18
was
originally
discovered
as
a
factor
that
enhanced
IFN-γ
production
from
anti-CD3-stimulated
Th1
cells,
especially
in
the
presence
of
IL-12.
Upon
stimulation
with
Ag
plus
IL-12,
naïve
T
cells
develop
into
IL-18
receptor
(IL-18R)
expressing
which
increase
response
to
stimulation.
Therefore,
IL-12
is
commitment
induces
development
cells.
In
contrast,
proinflammatory
cytokine
facilitates
type
1
responses.
However,
without
but
IL-2,
stimulates
NK
CD4+
NKT
and
established
produce
IL-3,
IL-9,
IL-13.
Furthermore,
together
mast
basophils
IL-4,
IL-13,
chemical
mediators
such
histamine.
various
cell
types
has
pleiotropic
functions.
member
IL-1
family
cytokines.
demonstrates
unique
function
by
binding
specific
expressed
on
this
review
article,
we
will
focus
features
health
disease
experimental
animals
humans.
Proceedings of the National Academy of Sciences,
Год журнала:
2016,
Номер
113(19)
Опубликована: Апрель 18, 2016
Significance
Dysfunction
of
the
innate
immune
system
is
involved
in
pathogenesis
Alzheimer’s
disease
(AD);
however,
pathophysiological
mechanisms
underlying
these
dysfunctions
are
unclear.
Here
we
report
that
stimulation
IL-33/ST2
signaling
rescues
memory
deficits
and
reduces
accumulation
β-amyloid
APP/PS1
mice
exhibit
select
pathologies
associated
with
AD.
Although
impaired
early
progression
AD,
IL-33
injection
contextual
mice.
skews
microglia
toward
an
alternative
activation
state
enhanced
Aβ
phagocytic
capacity
elevated
antiinflammatory
gene
expression,
which
results
a
decreased
proinflammatory
response
brain.
Thus,
this
study
suggests
can
be
developed
as
new
therapeutic
intervention
for
Clinical Science,
Год журнала:
2017,
Номер
131(16), С. 2183 - 2199
Опубликована: Июль 31, 2017
Chronic
diabetes
is
associated
with
metabolic
and
haemodynamic
stresses
which
can
facilitate
modifications
to
DNA,
proteins
lipids,
induce
cellular
dysfunction
damage,
stimulate
inflammatory
fibrotic
responses
lead
various
types
of
renal
injury.
Approximately
30–40%
patients
develop
nephropathy
this
injury
normally
progresses
in
about
a
third
patients.
Due
the
growing
incidence
diabetes,
diabetic
now
main
cause
end-stage
disease
(ESRD)
worldwide.
Accumulating
evidence
from
experimental
clinical
studies
has
demonstrated
that
inflammation
plays
critical
role
determining
whether
during
diabetes.
However,
immune
response
considerably
different
seen
autoimmune
kidney
diseases
or
acute
arising
episodes
ischaemia
infection.
This
review
evaluates
system
development
nephropathy,
including
specific
contributions
leucocyte
subsets
(macrophages,
neutrophils,
mast
cells,
T
B
lymphocytes),
danger-associated
molecular
patterns
(DAMPs),
inflammasomes,
immunoglobulin
complement.
It
also
examines
factors
may
influence
response,
genetic
exposure
other
insults.
In
addition,
discusses
therapies
are
currently
under
for
targeting
indicates
those
have
proceeded
into
trials.
Signal Transduction and Targeted Therapy,
Год журнала:
2022,
Номер
7(1)
Опубликована: Июнь 9, 2022
Abstract
Chronic
kidney
disease
(CKD)
is
a
chronic
renal
dysfunction
syndrome
that
characterized
by
nephron
loss,
inflammation,
myofibroblasts
activation,
and
extracellular
matrix
(ECM)
deposition.
Lipotoxicity
oxidative
stress
are
the
driving
force
for
loss
of
including
tubules,
glomerulus,
endothelium.
NLRP3
inflammasome
signaling,
MAPK
PI3K/Akt
RAAS
signaling
involves
in
lipotoxicity.
The
upregulated
Nox
expression
decreased
Nrf2
result
directly.
injured
resident
cells
release
proinflammatory
cytokines
chemokines
to
recruit
immune
such
as
macrophages
from
bone
marrow.
NF-κB
JAK-STAT
Toll-like
receptor
cGAS-STING
major
pathways
mediate
inflammation
inflammatory
cells.
produce
secret
great
number
profibrotic
TGF-β1,
Wnt
ligands,
angiotensin
II.
TGF-β
Notch
evoke
activation
promote
generation
ECM.
potential
therapies
targeted
these
also
introduced
here.
In
this
review,
we
update
key
lipotoxicity,
stress,
kidneys
with
injury,
drugs
based
on
latest
studies.
Unifying
will
be
instrumental
advance
further
basic
clinical
investigation
CKD.
International Journal of Molecular Sciences,
Год журнала:
2020,
Номер
21(11), С. 3798 - 3798
Опубликована: Май 27, 2020
Diabetic
nephropathy
(DN)
is
associated
with
an
increased
morbidity
and
mortality,
resulting
in
elevated
cost
for
public
health
systems.
DN
the
main
cause
of
chronic
kidney
disease
(CKD)
its
incidence
increases
number
patients
that
develop
end-stage
renal
(ESRD).
There
are
growing
epidemiological
preclinical
evidence
about
close
relationship
between
inflammatory
response
occurrence
progression
DN.
Several
anti-inflammatory
strategies
targeting
specific
mediators
(cell
adhesion
molecules,
chemokines
cytokines)
intracellular
signaling
pathways
have
shown
beneficial
effects
experimental
models
DN,
decreasing
proteinuria
lesions.
A
molecules
been
useful
to
identify
diabetic
at
high
risk
developing
complications.
In
this
review,
we
focus
on
key
role
inflammation
genesis
a
special
interest
effector
activated
leading
damage,
as
well
comprehensive
update
new
therapeutic
prevent
and/or
retard
injury.