Kidney Research and Clinical Practice,
Год журнала:
2020,
Номер
39(3), С. 244 - 258
Опубликована: Сен. 1, 2020
Mitochondria
are
energy-producing
organelles
that
not
only
satisfy
the
high
metabolic
demands
of
kidney
but
sense
and
respond
to
injury-induced
oxidative
stress
inflammation.
Kidneys
rich
in
mitochondria.
Mitochondrial
dysfunction
plays
a
critical
role
progression
acute
injury
chronic
disease.
responses
specific
stimuli
highly
regulated
synergistically
modulated
by
tightly
interconnected
processes,
including
mitochondrial
dynamics
(fission,
fusion)
mitophagy.
The
counterbalance
between
these
processes
is
essential
maintaining
healthy
network
Recent
literature
suggests
alterations
implicated
diseases.
A
decrease
fusion
promotes
fission-induced
fragmentation,
reduction
fission
produces
excessive
elongation.
removal
dysfunctional
mitochondria
mitophagy
crucial
for
their
quality
control.
Defective
function
disrupts
cellular
redox
potential
can
cause
cell
death.
DNA
derived
from
damaged
cells
also
act
as
damage-associated
molecular
patterns
recruit
immune
inflammatory
response
further
exaggerate
injury.
This
review
provides
comprehensive
overview
We
discuss
control
recent
advances
understanding
inflammation
tissue
damage
through
use
different
experimental
models
describe
mitochondria-targeted
therapeutic
approaches.
Keywords:
Acute
injury,
Inflammation,
Kidney
diseases,
Mitochondria,
Oxidative
Redox Biology,
Год журнала:
2020,
Номер
37, С. 101799 - 101799
Опубликована: Окт. 1, 2020
Oxidative
stress,
a
cytopathic
outcome
of
excessive
generation
ROS
and
the
repression
antioxidant
defense
system
for
elimination,
is
involved
in
pathogenesis
multiple
diseases,
including
diabetes
its
complications.
Retinopathy,
microvascular
complication
diabetes,
primary
cause
acquired
blindness
diabetic
patients.
stress
has
been
verified
as
one
critical
contributor
to
retinopathy.
can
both
contribute
result
from
metabolic
abnormalities
induced
by
hyperglycemia,
mainly
increased
flux
polyol
pathway
hexosamine
pathway,
hyper-activation
protein
kinase
C
(PKC)
isoforms,
accumulation
advanced
glycation
end
products
(AGEs).
Moreover,
hyperglycemia-mediated
epigenetic
modification
also
leads
imbalance
between
scavenging
production
ROS.
Excessive
induces
mitochondrial
damage,
cellular
apoptosis,
inflammation,
lipid
peroxidation,
structural
functional
alterations
retina.
Therefore,
it
important
understand
elucidate
oxidative
stress-related
mechanisms
underlying
progress
In
addition,
correlated
with
provide
potential
therapeutic
targets
develop
safe
effective
treatments
Here,
we
summarized
main
strategies
control
this
disease.
International Journal of Molecular Sciences,
Год журнала:
2020,
Номер
21(7), С. 2632 - 2632
Опубликована: Апрель 10, 2020
Lipotoxicity
is
characterized
by
the
ectopic
accumulation
of
lipids
in
organs
different
from
adipose
tissue.
mainly
associated
with
dysfunctional
signaling
and
insulin
resistance
response
non-adipose
tissue
such
as
myocardium,
pancreas,
skeletal
muscle,
liver,
kidney.
Serum
lipid
abnormalities
renal
have
been
development
kidney
diseases,
particular
diabetic
nephropathy.
Chronic
hyperinsulinemia,
often
seen
type
2
diabetes,
plays
a
crucial
role
blood
liver
metabolism
abnormalities,
thus
resulting
increased
non-esterified
fatty
acids
(NEFA).
Excessive
alters
cellular
homeostasis
activates
lipogenic
glycogenic
cell-signaling
pathways.
Recent
evidences
indicate
that
both
quantity
quality
are
involved
damage
to
lipotoxicity
activating
inflammation,
oxidative
stress,
mitochondrial
dysfunction,
cell-death.
The
pathological
effects
observed
cells,
promoting
podocyte
injury,
tubular
damage,
mesangial
proliferation,
endothelial
activation,
formation
macrophage-derived
foam
cells.
Therefore,
this
review
examines
recent
preclinical
clinical
research
about
potentially
harmful
kidney,
metabolic
markers
these
mechanisms,
major
pathways
affected,
causes
excessive
accumulation,
types
involved,
well
offers
comprehensive
update
therapeutic
strategies
targeting
lipotoxicity.
Frontiers in Endocrinology,
Год журнала:
2022,
Номер
13
Опубликована: Дек. 6, 2022
Objective
Diabetic
kidney
disease
(DKD)
is
the
most
common
chronic
(CKD)
and
has
highest
prevalence
of
end-stage
(ESKD)
globally,
owing
mostly
to
rise
in
Type
2
diabetes
mellitus
(T2DM)
correlated
with
obesity.
Current
research
suggested
that
immune
response
inflammation
may
play
a
role
pathophysiology
T2DM.
The
systemic
immune-inflammation
index
(SII)
novel
integrated
inflammatory
biomarker
not
yet
been
linked
DKD.
We
aimed
identify
potential
relationship
between
SII
Methods
In
National
Health
Nutrition
Examination
Survey
(NHANES)
2011
2018,
current
cross-sectional
study
was
conducted
among
adults
calculated
as
platelet
count
×
neutrophil
count/lymphocyte
count.
DKD
diagnosed
impaired
glomerular
filtration
rate
(<
60
mL/min/1.73
m
assessed
by
using
Chronic
Kidney
Disease
Epidemiology
Collaboration
algorithm),
albuminuria
(urine
albumin
creatinine
ratio
≥
30
mg/g),
or
both
T2DM
patients.
To
investigate
independent
association
DKD,
weighted
univariate
multivariable
logistic
regression
analyses
subgroup
were
performed.
Results
involved
3937
patients
total,
whom
1510
(38.4%)
had
for
diagnosis.
After
adjustment
covariates,
revealed
high
level
associated
increased
likelihood
(OR
=
1.42,
95%
CI:
1.10-1.83,
P
0.01).
Subgroup
interaction
tests
age,
gender,
estimated
(eGFR),
urine
albumin-to-creatinine
(ACR),
body
mass
(BMI),
hypertension,
hyperlipidemia,
anti-inflammation
therapy
(yes
no),
metformin
use
insulin
no)
no
significant
dependence
on
this
positive
(all
p
>0.05).
Conclusions
Our
results
indicate
higher
could
be
cost-effective
straightforward
approach
detecting
This
needs
verified
further
prospective
investigations.
Cell Death and Disease,
Год журнала:
2021,
Номер
12(10)
Опубликована: Окт. 9, 2021
Abstract
Renal
tubulointerstitial
fibrosis
was
a
crucial
pathological
feature
of
diabetic
nephropathy
(DN),
and
renal
tubular
injury
might
associate
with
abnormal
mitophagy.
In
this
study,
we
investigated
the
effects
molecular
mechanisms
AMPK
agonist
metformin
on
mitophagy
cellular
in
cell
under
condition.
The
high
fat
diet
(HFD)
streptozotocin
(STZ)-induced
type
2
mice
model
HK-2
cells
were
used
study.
Metformin
administered
drinking
water
(200
mg/kg/d)
for
24
weeks.
lesions,
oxidative
stress
some
indicators
(e.g.,
LC3II,
Pink1,
Parkin)
examined
both
tissue
cells.
Additionally,
compound
C
(an
inhibitor)
Pink1
siRNA
applied
to
explore
regulation
mechanism
We
found
that
expression
p-AMPK,
Parkin,
Atg5
decreased
obviously.
reduced
levels
serum
creatinine,
urine
protein,
attenuated
HFD/STZ
induced
mice.
addition,
reversed
dysfunction
over-expression
NLRP3.
vitro
pretreatment
inhibitor
or
negated
beneficial
metformin.
Furthermore,
noted
activated
p-AMPK
promoted
translocation
from
cytoplasm
mitochondria,
then
occurrence
HG/HFA
ambience.
Our
results
suggested
first
time
ameliorated
HFD/STZ-induced
via
activating
through
p-AMPK-Pink1-Parkin
pathway.
