Diagnostics,
Journal Year:
2025,
Volume and Issue:
15(8), P. 973 - 973
Published: April 11, 2025
Diabetes
mellitus
(DM)
has
emerged
as
the
most
common
cause
of
chronic
kidney
disease
(CKD)
and
end-stage
renal
(ESRD)
globally
in
recent
years.
Diabetic
nephropathy
(DN),
or
diabetic
(DKD)
that
occurs
a
direct
consequence
DM,
complex
pathophysiological
mechanisms,
such
various
inflammatory
processes
genetic
epigenetic
factors,
often
accentuated
by
comorbid
illnesses
like
hypertension
dyslipidemia.
Therefore,
management
DKD
involves
targeting
these
etio-pathological
processes.
Various
medications
with
remarkable
modifying
properties
have
been
introduced
for
treatment
DN
We
update
current
future
diagnostic
therapeutic
landscapes
against
this
article.
Frontiers in Endocrinology,
Journal Year:
2024,
Volume and Issue:
15
Published: April 5, 2024
Diabetic
vascular
complications
are
prevalent
and
severe
among
diabetic
patients,
profoundly
affecting
both
their
quality
of
life
long-term
prospects.
These
can
be
classified
into
macrovascular
microvascular
complications.
Under
the
impact
risk
factors
such
as
elevated
blood
glucose,
pressure,
cholesterol
lipids,
endothelium
undergoes
endothelial
dysfunction,
characterized
by
increased
inflammation
oxidative
stress,
decreased
NO
biosynthesis,
endothelial-mesenchymal
transition,
senescence,
even
cell
death.
processes
will
ultimately
lead
to
diseases,
with
diseases
mainly
atherosclerosis
(AS)
thickening
basement
membrane.
It
further
indicates
a
primary
contributor
morbidity
mortality
observed
in
individuals
diabetes.
In
this
review,
we
delve
intricate
mechanisms
that
drive
dysfunction
during
diabetes
progression
its
associated
Furthermore,
outline
various
pharmacotherapies
targeting
hope
accelerating
effective
therapeutic
drug
discovery
for
early
control
Molecular Biomedicine,
Journal Year:
2025,
Volume and Issue:
6(1)
Published: March 22, 2025
Abstract
Klotho,
initially
introduced
as
an
anti-aging
protein,
is
expressed
in
the
brain,
pancreas,
and
most
prominently
kidney.
The
two
forms
of
Klotho
(membrane-bound
soluble
form)
have
diverse
pharmacological
functions
such
anti-inflammatory,
anti-oxidative,
anti-fibrotic,
tumour-suppressive
etc.
membrane-bound
form
plays
a
pivotal
role
maintaining
kidney
homeostasis
by
regulating
fibroblast
growth
factor
23
(FGF
23)
signalling,
vitamin
D
metabolism
phosphate
balance.
deficiency
has
been
linked
with
significantly
reduced
protection
against
various
pathological
phenotypes,
including
diabetic
disease
(DKD),
which
major
cause
chronic
leading
to
end-stage
disease.
Owing
pleiotropic
actions
klotho,
it
shown
beneficial
effects
DKD
tackling
complex
pathophysiology
reducing
inflammation,
oxidative
stress,
well
fibrosis.
Moreover,
protective
effect
klotho
extends
beyond
other
conditions,
cardiovascular
diseases,
alzheimer's
disease,
cancer,
inflammatory
bowel
liver
Therefore,
this
review
summarizes
relationship
between
expression
diseases
special
emphasis
on
DKD,
distinct
mechanisms
potential
exogenous
supplementation
therapeutic
strategy.
Future
research
into
could
unravel
novel
treatment
avenues
for
diseases.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(7), P. 3969 - 3969
Published: April 3, 2024
Diabetic
kidney
disease
(DKD)
is
a
chronic
microvascular
complication
in
patients
with
diabetes
mellitus
(DM)
and
the
leading
cause
of
end-stage
(ESKD).
Although
glomerulosclerosis,
tubular
injury
interstitial
fibrosis
are
typical
damages
DKD,
interplay
different
processes
(metabolic
factors,
oxidative
stress,
inflammatory
pathway,
fibrotic
signaling,
hemodynamic
mechanisms)
appears
to
drive
onset
progression
DKD.
A
growing
understanding
pathogenetic
mechanisms,
development
new
therapeutics,
opening
way
for
era
nephroprotection
based
on
precision-medicine
approaches.
This
review
summarizes
therapeutic
options
linked
specific
molecular
mechanisms
including
renin-angiotensin-aldosterone
system
blockers,
SGLT2
inhibitors,
mineralocorticoid
receptor
antagonists,
glucagon-like
peptide-1
agonists,
endothelin
aldosterone
synthase
inhibitors.
In
nephroprotection,
these
drugs,
as
pillars
personalized
medicine,
can
improve
renal
outcomes
enhance
quality
life
individuals
World Journal of Diabetes,
Journal Year:
2025,
Volume and Issue:
16(4)
Published: Feb. 28, 2025
In
this
editorial,
we
discussed
the
article
published
in
recent
issue
of
World
Journal
Diabetes.
To
understand
effect
mizagliflozin
on
kidney
injury
induced
by
diabetes,
focused
mechanisms
which
high
glucose
triggers
oxidative
stress
and
contributes
to
diabetes.
The
level
unmetabolized
reaching
reabsorption
renal
tubules,
elevates
cellular
cells.
High
induces
lactate
dehydrogenase
overexpression
thus
shifts
metabolism,
causes
mitochondrial
dysfunction.
Mitochondria
generate
approximately
90%
reactive
oxygen
species
cells,
whose
dysfunction
further
alters
metabolism
enhances
generation.
Oxidative
stimulates
proinflammatory
factor
production
inflammatory
injury.
Mizagliflozin
decreases
ameliorates
diabetes-induced
Drug Design Development and Therapy,
Journal Year:
2024,
Volume and Issue:
Volume 18, P. 1439 - 1457
Published: April 1, 2024
Background:
Acteoside,
an
active
ingredient
found
in
various
medicinal
herbs,
is
effective
the
treatment
of
diabetic
kidney
disease
(DKD);
however,
intrinsic
pharmacological
mechanism
action
acteoside
DKD
remains
unclear.
This
study
utilizes
a
combined
approach
network
pharmacology
and
experimental
validation
to
investigate
potential
molecular
systematically.
Methods:
First,
targets
DKD-associated
were
aggregated
from
public
databases.
Subsequently,
utilizing
protein-protein
interaction
(PPI)
networks,
alongside
GO
KEGG
pathway
enrichment
analyses,
we
established
target-pathway
networks
identify
core
therapeutic
pathways.
Further,
docking
facilitated
confirmation
interactions
between
central
targets.
Finally,
conjectured
mechanisms
against
verified
through
experimentation
on
unilateral
nephrectomy
with
streptozotocin
(STZ)
rat
model.
The
underlying
downstream
further
investigated.
Results:
Network
identified
129
intersected
for
treatment,
including
such
as
AKT1,
TNF,
Casp3,
MMP9,
SRC,
IGF1,
EGFR,
HRAS,
CASP8,
MAPK8.
Enrichment
analyses
indicated
PI3K-Akt,
MAPK,
Metabolic,
Relaxin
signaling
pathways
could
be
involved
this
context.
Molecular
revealed
high-affinity
binding
PIK3R1,
NF-κB1.
In
vivo
studies
validated
efficacy
acteoside,
demonstrating
reduced
blood
glucose
levels,
improved
serum
Scr
BUN
decreased
24-hour
urinary
total
protein
(P<
0.05),
mitigated
podocyte
injury
0.05)
ameliorated
renal
pathological
lesions.
Furthermore,
finding
indicates
that
inhibits
expression
pyroptosis
markers
NLRP3,
Caspase-1,
IL-1β,
IL-18
modulation
PI3K/AKT/NF-κB
pathway.
Conclusion:
Acteoside
demonstrates
renoprotective
effects
by
regulating
alleviating
pyroptosis.
explores
acteoside's
providing
foundation
basic
clinical
research.
Keywords:
DKD,
pharmacology,
verification
Journal of Clinical Medicine,
Journal Year:
2025,
Volume and Issue:
14(4), P. 1088 - 1088
Published: Feb. 8, 2025
Background:
Excessive
accumulation
of
glomerular
extracellular
matrix
(ECM)
is
a
key
factor
in
the
development
and
progression
diabetic
nephropathy
(DN).
As
kidney
dysfunction
has
been
reported
normoalbuminuric
patients,
identifying
novel
diagnostic
prognostic
markers
essential
for
prevention
treatment
DN.
Methods:
Urinary
excretion
neutrophil
gelatinase-associated
lipocalin
(NGAL)
ECM-related
glycoproteins,
i.e.,
fibronectin
(FN)
laminin
(LN),
was
measured
obese
patients
with
newly
diagnosed
type
2
diabetes
mellitus
(T2DM)
before
after
6
months
metformin
therapy.
Results:
Baseline
NGAL
(1.27
(0.80–2.36)
ng/mg
Cr),
FN
(11.19
(5.31–21.56)
Cr)
LN
(123.17
(54.56–419.28)
pg/mg
levels
did
not
significantly
differ
between
T2DM
controls
(1.95
(1.09–2.97)
Cr,
11.94
(7.78–18.01)
Cr
157.85
(83.75–326.40)
respectively).
In
multivariate
regression
analysis,
body
mass
index
identified
as
only
significant
predictor
influencing
urinary
at
baseline,
β
=
0.249,
p
0.005
1.068,
0.010,
respectively.
Metformin
increased
both
ECM
proteins,
(18.48
(11.64–32.46)
(179.51
(106.22–414.68)
without
any
effect
on
(1.44
(0.81–2.72)
Cr).
were
positively
associated
(r
0.709
r
0.646,
<
0.001,
respectively)
0.594
0.479,
No
correlations
found
NGAL,
FN,
LN,
albuminuria.
However,
correlated
albumin/creatinine
ratio
(ACR)
0.323,
0.05)
0.287,
therapy,
negatively
estimated
filtration
rate
(eGFR)
pre-treatment
diabetics
−0.290,
0.05).
also
ACR
0.384,
0.01
0.470,
0.001),
although
association
limited
to
untreated
0.422,
0.01).
Conclusions:
Our
results
suggest
that
beneficial
turnover
increase
non-collagenous
injury,
LN.
Additionally,
may
serve
useful
tools
monitoring
early
renal
injury
patients.
Journal of Diabetes,
Journal Year:
2025,
Volume and Issue:
17(2)
Published: Feb. 1, 2025
ABSTRACT
Objective
This
study
aims
to
explore
the
link
between
iron
deficiency
anemia
(IDA)
and
diabetic
kidney
disease
(DKD)
assess
safety
of
supplementation.
It
also
investigates
key
mechanisms
molecules
involved
in
deficiency's
role
development.
Methods
A
retrospective
analysis
was
conducted
on
1,398
T2DM
patients
using
propensity
score
matching
identify
risk
factors
for
DKD.
Mendelian
randomization
(MR)
used
causal
relationships
IDA,
supplementation,
liver
content,
The
GSE27999
dataset
analyzed
examine
how
an
iron‐deficient
diet
affects
kidney‐related
gene
expression.
Key
pathways
were
identified
through
GSEA,
GO/KEGG,
PPI
analysis.
Results
Retrospective
data
showed
a
correlation
hemoglobin
levels
DKD
risk.
Logistic
regression
confirmed
that
IDA
increased
independently
other
factors.
MR
revealed
DKD,
with
no
significant
effect
from
580
differentially
expressed
genes,
enriched
like
cytokine
signaling,
oxidative
biology,
small
molecule
transport.
highlighted
10
hub
including
Cyp2d26
Fgf4.
Conclusion
increases
susceptibility
possibly
stress
altered
However,
supplementation
does
not
appear
increase
Journal of Clinical & Translational Endocrinology,
Journal Year:
2025,
Volume and Issue:
40, P. 100387 - 100387
Published: March 2, 2025
In
diabetic
kidney
disease
(DKD),
urinary
decoy
receptor
2
(uDcR2)
levels
are
associated
with
tubulointerstitial
fibrosis;
however,
whether
uDcR2
can
predict
renal
outcomes
remains
unclear.
Herein,
we
analyzed
the
association
between
and
(defined
as
a
composite
of
serum
creatinine
(SCr)
increase
50
%
from
baseline,
or
initiation
dialysis
for
end-stage
disease)
in
153
patients
biopsy-proven
DKD.
Patients
were
divided
into
(n
=
67)
no
86)
outcome
groups.
measured
using
ELISA.
The
area
under
receiver
operating
characteristic
curve
(AUC)
discriminating
DKD
was
calculated.
Kaplan-Meier
survival
analysis
multifactorial
Cox
regression
models
evaluated
outcomes.
Renal
DcR2
mRNA
protein
expression
detected
situ
hybridization
immunohistochemical
staining.
Immunofluorescence
revealed
α-SMA
colocalization.
uDcR2/Cr
higher
than
group.
positively
correlated
ACR,
SCr,
interstitial
fibrosis
tubular
atrophy
(IFTA),
negatively
eGFR.
had
an
AUC
0.825
at
optimal
cut-off
value
389
ng/gCr.
Addition
to
eGFR,
IFTA
improved
predictions.
significantly
lower
≥
group
level
percentages.
increased
DcR2-positive
tubules
their
surroundings.
Overall,
is
independent
predictor
outcomes,
potential
improving
prevention
treatment
