Kidney International Reports,
Journal Year:
2024,
Volume and Issue:
9(7), P. 1972 - 1985
Published: April 3, 2024
Diabetes
mellitus
presents
a
significant
threat
to
human
health
because
it
disrupts
energy
metabolism
and
gives
rise
various
complications,
including
diabetic
kidney
disease
(DKD).
Metabolic
adaptations
occurring
in
the
response
diabetes
contribute
pathogenesis
of
DKD.
Iron
ferroptosis,
recently
defined
form
cell
death
resulting
from
iron-dependent
excessive
accumulation
lipid
peroxides,
have
emerged
as
crucial
players
progression
In
this
comprehensive
review,
we
highlight
profound
impact
adaptive
maladaptive
responses
regulating
iron
on
damage
diabetes.
We
summarize
current
understanding
homeostasis
ferroptosis
Finally,
propose
that
precise
manipulation
may
serve
potential
strategies
for
management
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(11), P. 9352 - 9352
Published: May 27, 2023
This
review
focuses
on
the
multiple
and
reciprocal
relationships
that
exist
between
oxidative
stress,
hyperglycemia
diabetes
related
metabolic
disorders.
Human
metabolism
uses
most
of
consumed
glucose
under
aerobic
conditions.
Oxygen
is
needed
in
mitochondria
to
obtain
energy,
as
well
for
action
microsomal
oxidases
cytosolic
pro-oxidant
enzymes.
relentlessly
generates
a
certain
amount
reactive
oxygen
species
(ROS).
Although
ROS
are
intracellular
signals
necessary
some
physiological
processes,
their
accumulation
leads
hyperglycemia,
progressive
resistance
insulin.
A
cellular
versus
an
antioxidant
equilibrium
would
regulate
levels,
but
pro-inflammatory
conditions
feed
back
each
other
relevance
interconnections
tends
increase
those
Hyperglycemia
promotes
collateral
through
protein
kinase
C,
polyols
hexosamine
routes.
In
addition,
it
also
facilitates
spontaneous
auto-oxidation
formation
advanced
glycation
end
products
(AGEs),
which
turn
interact
with
receptors
(RAGE).
The
mentioned
processes
undermine
structures,
finally
giving
place
progressively
greater
degree
stress
further
alterations,
complications.
NFκB
major
transcription
factor
involved
expression
mediators,
while
Nrf2
regulating
response.
FoxO
equilibrium,
its
role
controversial.
summarizes
key
factors
linking
diverse
routes
enhanced
vice
versa,
emphasizing
desirable
balance
proteins.
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(4), P. 455 - 455
Published: April 12, 2024
Diabetic
kidney
disease
(DKD)
is
the
principal
culprit
behind
chronic
(CKD),
ultimately
developing
end-stage
renal
(ESRD)
and
necessitating
costly
dialysis
or
transplantation.
The
limited
therapeutic
efficiency
among
individuals
with
DKD
a
result
of
our
finite
understanding
its
pathogenesis.
complex
interactions
between
various
factors.
Oxidative
stress
fundamental
factor
that
can
establish
link
hyperglycemia
vascular
complications
frequently
encountered
in
diabetes,
particularly
DKD.
It
crucial
to
recognize
essential
integral
role
oxidative
development
diabetic
complications,
Hyperglycemia
primary
trigger
an
upsurge
production
reactive
oxygen
species
(ROS),
sparking
stress.
main
endogenous
sources
ROS
include
mitochondrial
production,
NADPH
oxidases
(Nox),
uncoupled
endothelial
nitric
oxide
synthase
(eNOS),
xanthine
oxidase
(XO),
cytochrome
P450
(CYP450),
lipoxygenase.
Under
persistent
high
glucose
levels,
immune
cells,
complement
system,
advanced
glycation
end
products
(AGEs),
protein
kinase
C
(PKC),
polyol
pathway,
hexosamine
pathway
are
activated.
Consequently,
oxidant–antioxidant
balance
within
body
disrupted,
which
triggers
series
reactions
downstream
pathways,
including
phosphoinositide
3-kinase/protein
B
(PI3K/Akt),
transforming
growth
beta/p38-mitogen-activated
(TGF-β/p38-MAPK),
nuclear
kappa
(NF-κB),
adenosine
monophosphate-activated
(AMPK),
Janus
kinase/signal
transducer
activator
transcription
(JAK/STAT)
signaling.
might
persist
even
if
strict
control
achieved,
be
attributed
epigenetic
modifications.
treatment
remains
unresolved
issue.
Therefore,
reducing
intriguing
target.
clinical
trials
have
shown
bardoxolone
methyl,
erythroid
2-related
2
(Nrf2)
activator,
blood
glucose-lowering
drugs,
such
as
sodium-glucose
cotransporter
inhibitors,
glucagon-like
peptide-1
receptor
agonists
effectively
slow
down
progression
by
Other
antioxidants,
vitamins,
lipoic
acid,
Nox
regulators,
present
promising
option
for
In
this
review,
we
conduct
thorough
assessment
both
preclinical
studies
current
findings
from
focus
on
targeted
interventions
aimed
at
manipulating
these
pathways.
We
aim
provide
comprehensive
overview
state
research
area
identify
key
areas
future
exploration.
Cardiovascular Diabetology,
Journal Year:
2024,
Volume and Issue:
23(1)
Published: April 25, 2024
Abstract
Background
This
study
was
designed
to
assess
the
associations
between
emerging
cardiometabolic
indices—the
atherogenic
index
of
plasma
(AIP),
stress
hyperglycemia
ratio
(SHR),
triglyceride-glucose
(TyG)
index,
and
homeostasis
model
assessment
insulin
resistance
(HOMA-IR)—and
incidence
diabetic
kidney
disease
(DKD)
in
type
2
diabetes
(T2D)
patients.
Methods
We
consecutively
enrolled
4351
T2D
The
AIP,
SHR,
TyG
HOMA-IR
were
calculated
from
baseline
parameters.
DKD
defined
as
a
urine
albumin/creatinine
>
30
mg/g
or
an
eGFR
<
60
mL/min
per
1.73
m.
All
participants
categorized
into
tertiles
based
on
indices.
Multivariate
logistic
regression
models,
restricted
cubic
splines,
receiver
operating
characteristic
(ROC)
curves
used
for
analysis.
Results
A
total
1371
(31.5%)
patients
diagnosed
with
DKD.
spline
showed
J-shaped
association
AIP
DKD,
log-shaped
U-shaped
SHR
incidence.
revealed
that
individuals
highest
tertile
four
indices
had
significantly
greater
risk
than
did
those
lowest
(AIP:
OR
=
1.08,
95%
CI
1.02–1.14,
P
0.005;
SHR:
1.42,
1.12–1.81,
0.004;
index:
1.86,
1.42–2.45,
0.001;
HOMA-IR:
2.24,
1.52–3.30,
0.001).
score
better
other
at
predicting
optimal
cutoff
3.532.
Conclusions
Elevated
are
associated
T2D.
Among
these
indices,
demonstrated
strongest
predictive
value
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
24(1), P. 570 - 570
Published: Dec. 29, 2022
Diabetic
kidney
disease
(DKD)
is
the
leading
cause
of
chronic
disease,
including
end-stage
and
increases
risk
cardiovascular
mortality.
Although
treatment
options
for
DKD,
angiotensin-converting
enzyme
inhibitors,
angiotensin
II
receptor
blockers,
sodium-glucose
cotransporter
2
mineralocorticoid
antagonists,
have
advanced,
their
efficacy
still
limited.
Thus,
a
deeper
understanding
molecular
mechanisms
DKD
onset
progression
necessary
development
new
innovative
treatments
DKD.
The
complex
pathogenesis
includes
various
different
pathways,
can
be
broadly
classified
into
inflammatory,
fibrotic,
metabolic,
hemodynamic
factors.
Here,
we
summarize
recent
findings
in
basic
research,
focusing
on
each
factor
advances
Collective
evidence
from
clinical
research
studies
helpful
definitive
regulatory
systems.
Further
comprehensive
exploration
warranted
to
advance
our
knowledge
establish
novel
preventive
strategies.
Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
14
Published: Jan. 8, 2024
Rhodiola
rosea
is
a
valuable
functional
medicinal
plant
widely
utilized
in
China
and
other
Asian
countries
for
its
anti-fatigue,
anti-aging,
altitude
sickness
prevention
properties.
Salidroside,
most
active
constituent
derived
from
,
exhibits
potent
antioxidative,
hypoxia-resistant,
anti-inflammatory,
anticancer,
anti-aging
effects
that
have
garnered
significant
attention.
The
appreciation
of
the
pharmacological
role
salidroside
has
burgeoned
over
last
decade,
making
it
beneficial
option
treatment
multiple
diseases,
including
atherosclerosis,
Alzheimer’s
disease,
Parkinson’s
cardiovascular
more.
With
renoprotective
effects,
parallel
with
inhibition
oxidative
stress
inflammation,
holds
promise
as
potential
therapeutic
agent
kidney
damage.
This
article
provides
an
overview
microinflammatory
state
disease
discuss
current
strategies,
particular
focus
on
highlighting
recent
advancements
utilizing
renal
disease.
mechanisms
action
are
primarily
associated
regulation
gene
protein
expression
glomerular
endothelial
cells,
podocytes,
tubule
mesangial
cells
cell
carcinoma
cell,
TNF-α,
TGF-β,
IL-1β,
IL-17A,
IL-6,
MCP-1,
Bcl-2,
VEGF,
ECM
protein,
caspase-3,
HIF-1α,
BIM,
well
modulation
AMPK/SIRT1,
Nrf2/HO-1,
Sirt1/PGC-1α,
ROS/Src/Cav-1,
Akt/GSK-3β,
TXNIP-NLRP3,
ERK1/2,
TGF-β1/Smad2/3,
PI3K/Akt,
Wnt1/Wnt3a
β-catenin,
TLR4/NF-κB,
MAPK,
JAK2/STAT3,
SIRT1/Nrf2
pathways.
To
best
our
knowledge,
this
review
first
to
comprehensively
cover
protective
diverse
suggests
great
be
developed
drug
metabolic
syndrome,
cerebrovascular
diseases
complications.
Biomedicine & Pharmacotherapy,
Journal Year:
2024,
Volume and Issue:
177, P. 117008 - 117008
Published: June 19, 2024
Astragaloside
IV
(AS-IV)
exhibits
diverse
biological
activities.
Despite
this,
the
detailed
molecular
mechanisms
by
which
AS-IV
ameliorates
diabetic
nephropathy
(DN)
and
shields
podocytes
from
oxidative
stress
(OS)
mitochondrial
dysfunction
remain
poorly
understood.
In
this
study,
we
used
biochemical
assays,
histopathological
analysis,
Doppler
ultrasound,
transmission
electron
microscopy，flow
cytometry,
fluorescence
staining,
Western
blotting
other
methods.
was
administered
to
db/db
mice
for
in
vivo
experimentation.
Our
findings
indicated
that
treatment
significantly
reduced
diabetes-associated
markers,
proteinuria,
kidney
damage.
It
also
diminished
ROS
levels
kidney,
enhanced
expression
of
endogenous
antioxidant
enzymes,
improved
health.
Phenyl
sulfate
(PS),
a
protein-bound
uremic
solute
enteric
origin,
has
been
closely
linked
with
DN
represents
promising
avenue
further
research.
vitro,
PS
exposure
induced
OS
podocytes,
increasing
while
decreasing
enzyme
activity
(Catalase,
Heme
Oxygenase-1,
Superoxide
Dismutase,
Glutathione
Peroxidase).
inhibitors
(N-acetyl-L-cysteine,
NAC)
as
positive
control
group
can
reduce
restore
enzymes
protein
levels.
Additionally,
markers
associated
biosynthesis
function
(SIRT1,
PGC1α,
Nrf1,
TFAM).
These
adverse
effects
were
partially
reversed
treatment.
However,
co-treatment
SIRT1
inhibitor
EX527
failed
these
indicators.
Overall,
our
study
demonstrates
effectively
attenuates
mitigates
PS-induced
via
SIRT1/PGC1α/Nrf1
pathway.
