Regulatory Mechanisms in Biosystems,
Год журнала:
2024,
Номер
15(4), С. 962 - 969
Опубликована: Ноя. 18, 2024
Deep
deteriorations
accompany
diabetes
in
all
types
of
metabolism
with
an
impact
on
functional
activity
and
complications
that
are
vital
significance.
Damage
to
the
liver
contributes
worsening
patient's
state.
Oxidative
stress
makes
a
pivotal
contribution
diabetes-induced
disorders.
The
investigation
niacin-oxyethylidene-diphosphonate
germanate
(MIGU-4)
α-lipoic
acid
treatment,
which
both
possessed
antioxidative
properties
upon
state
rats
streptozotocin
induced
diabetes,
was
aim
investigation.
Treatment
MIGU-4
(25.0
mg/kg,
i.p.)
(50.0
started
six
weeks
after
induction
by
(65.0
administration.and
performed
daily
for
further
weeks.
results
obtained
revealed
combined
administration
mg/kg)
caused
increase
albumin
decrease
bilirubin
when
compared
streptozotocin-treated
rats.
Administration
reduction
cholesterol
triglycerides,
low-density
lipoproteins,
while
high-density
lipoproteins
increased.
Besides,
treatment
reduced
malone
dialdehyde,
increased
glutathione
content,
superoxide
dismutase
catalase
streptozotocin-diabetes.
protective
effect
is
more
pronounced
than
alone.
There
ample
scope
investigations
treating
damage
complex
metabolic
Frontiers in Nephrology,
Год журнала:
2025,
Номер
5
Опубликована: Янв. 23, 2025
Background
Glomerular
diseases
significantly
impact
global
health.
This
study
investigated
public
interest
in
five
common
glomerular
diseases.
Methods
Google
Trends™
were
used
to
analyze
search
activity
from
January
2004
December
2024
for
IgA
nephropathy
(IgAN),
membranous
glomerulonephritis
(MN),
focal
segmental
glomerulosclerosis
(FSGS),
lupus
nephritis
(LN),
and
diabetic
(DN).
Data
retrieved
both
globally
English-speaking
countries,
including
the
United
States.
Monthly
yearly
relative
assessed
compared.
Results
Globally,
IgAN
had
highest
average
activity,
followed
by
DN,
FSGS,
LN,
MN.
Both
FSGS
exhibited
declining
trends,
while
LN
showed
an
upward
pattern.
MN
DN
experienced
a
modest
decline
before
2016,
preceded
slight
increase.
Among
was
predominantly
concentrated
primarily
States,
Kingdom,
Canada,
Australia,
with
States
consistently
ranking
as
leading
country.
For
IgAN,
MN,
trends
observed
appeared
align
data.
In
contrast,
exceeded
levels,
slightly
lower
than
activity.
most
prominent
North
Dakota,
Massachusetts,
Delaware,
respectively,
saw
peak
West
Virginia.
Conclusion
Public
engagement
has
not
uniformly
grown,
at
least
emphasizing
need
enhanced
awareness
efforts.
Future
analysis
should
prioritize
terms
predominant
language
of
each
Objectives
Diabetic
kidney
disease
(DKD)
is
driven
by
mitochondrial
dysfunction
and
immune
dysregulation,
yet
the
mechanistic
interplay
remains
poorly
defined.
This
study
aimed
to
identify
key
molecular
networks
linking
pathways
DKD
progression,
with
a
focus
on
uncovering
biomarkers
therapeutic
targets.
Diabetic
nephropathy
(DN)
is
a
common
microvascular
complication
of
diabetes.
Mitochondrial
dysfunction
in
the
kidney
caused
by
diabetes
has
previously
been
linked
to
pathogenesis
DN.
By
mass
spectrometry,
we
identified
characteristic
proteins
DN
from
renal
mitochondria
mouse
model.
To
identify
core
among
them,
Mendelian
randomization
(MR)
analysis,
microarray
data
validation,
and
drug-target
interaction
analysis
were
employed.
MR
found
that
189
candidate
targets
had
causal
link
with
risk
factors
(estimated
glomerular
filtration
rate
(eGFR),
urinary
albumin
excretion,
serum
creatinine).
After
systematic
validated
SLC25A16,
CTNND1,
C2CD2L,
ALDH3A2,
NEU1,
APEH,
CORO1A,
NUDT19,
NDUFA4L2
are
promising
druggability
This
study
suggests
feasibility
using
for
drug
target
screening,
provides
potential
insights
into
mitochondrial
research,
which
may
contribute
further
exploration.
Frontiers in Physiology,
Год журнала:
2025,
Номер
16
Опубликована: Апрель 10, 2025
Background
Diabetic
nephropathy
(DN),
a
leading
cause
of
end-stage
renal
disease,
exerts
substantial
burden
on
healthcare
systems
globally.
Emerging
evidence
highlights
ferroptosis
-
an
iron-dependent
form
cell
death
driven
by
lipid
peroxidation
and
glutathione
depletion
as
critical
contributor
to
DN
progression
via
oxidative
stress,
tubular
injury,
glomerular
dysfunction.
Despite
increasing
research
interest,
comprehensive
synthesis
trends
mechanistic
insights
is
lacking.
Objective
This
study
integrated
bibliometric
analysis
with
review
map
the
evolving
landscape
in
DN,
identify
hotspots,
propose
future
directions
for
therapeutic
development.
Methods
In
total,
86
publications
(2018–2023)
were
retrieved
from
Web
Science
Core
Collection
analyzed
using
CiteSpace
VOSviewer.
Co-occurrence
networks,
citation
trends,
keyword
bursts
examined
delineate
global
contributions,
collaborative
emerging
themes.
Results
Annual
publication
numbers
surged
12-fold
after
2020,
China
contributing
highest
proportion
(60.4%),
led
institutions
such
Zhengzhou
University.
The
United
States
America
Germany
showed
high
centrality
networks.
Key
themes
included
peroxidase
4
(GPX4)-mediated
antioxidant
defenses,
acyl-CoA
synthetase
long-chain
family
member
(ACSL4)-mediated
remodeling,
iron
dysregulation.
Frontiers
Endocrinology
(nine
articles)
Free
Radical
Biology
Medicine
(highest
count:
171)
emerged
pivotal
platforms.
Mechanistic
analyses
identified
three
defense
axes
(GPX4,
FSP1/CoQ10,
GCH1/BH4)
type-specific
vulnerabilities
tubular,
podocyte,
endothelial
cells.
Preclinical
agents,
including
ginkgolide
B
(GB)
dapagliflozin,
effectively
restored
homeostasis
attenuated
damage.
Conclusion
Ferroptosis
promising
target
yet
its
clinical
translation
remains
infancy.
Future
efforts
should
prioritize
large-scale
trials,
single-cell
profiling,
interdisciplinary
integration
bridge
molecular
precision
therapies.
provides
roadmap
advancing
ferroptosis-targeted
interventions
emphasizing
collaborations
biomarker-driven
strategies.
Hormone and Metabolic Research,
Год журнала:
2024,
Номер
unknown
Опубликована: Ноя. 21, 2024
Abstract
Diabetic
nephropathy
represents
a
predominant
etiology
of
end-stage
renal
disease
(ESRD)
on
global
scale,
significantly
impacting
the
morbidity
and
mortality
rates
individuals
with
diabetes.
The
primary
objective
this
analysis
is
to
furnish
comprehensive
examination
etiology,
fundamental
mechanisms,
treatment
modalities
for
DN.
development
DN
stems
from
multitude
factors,
encompassing
intricate
interplay
involving
metabolic
irregularities
induced
by
hyperglycemia,
alterations
in
hemodynamics,
inflammatory
responses,
oxidative
stress,
genetic
susceptibility.
Principal
mechanisms
encompass
generation
advanced
glycation
end
products
(AGEs),
activation
protein
kinase
C
(PKC),
overexpression
renin-angiotensin-aldosterone
system
(RAAS).
These
processes
precipitate
glomerular
hyperfiltration,
hypertrophy,
eventually,
fibrosis
scarring
parenchyma.
Initially,
hyperglycemia
triggers
mesangial
proliferation
thickening
basement
membrane
incipient
stages
DN,
subsequently
leading
progressive
sclerosis
tubulointerstitial
fibrosis.
Inflammatory
cascades,
notably
cytokines
like
TGF-β
NF-κB,
play
pivotal
roles
advancement
fostering
accumulation
extracellular
matrix
Inflammation
pathways,
particularly
those
essential
diabetic
progression
stimulating
presence
worsened
dysfunctional
mitochondria,
contributes
further
injury
via
lipid
peroxidation
DNA
damage.
Current
therapeutic
approaches
concentrate
optimizing
glycemic
control,
controlling
hypertension,
suppressing
system.
Among
antihypertensive
medications,
ACE
inhibitors
angiotensin
II
receptor
blockers
are
crucial
decelerating
advancement.
Cell Biology International,
Год журнала:
2024,
Номер
48(9), С. 1240 - 1253
Опубликована: Июнь 30, 2024
Abstract
Diabetic
nephropathy
(DN)
is
the
predominant
secondary
resulting
in
global
end‐stage
renal
disease.
It
attracting
significant
attention
both
domestic
and
international
research
due
to
its
widespread
occurrence,
fast
advancement,
limited
choices
for
prevention
treatment.
The
pathophysiology
of
this
condition
intricate
involves
multiple
molecular
cellular
pathways
at
various
levels.
This
article
provides
a
concise
overview
processes
involved
development
DN.
discusses
factors,
such
as
signaling
pathways,
cytokines,
inflammatory
responses,
oxidative
stress,
damage,
autophagy,
epigenetics.
aim
offer
clinicians
valuable
reference
DN's
diagnosis,
treatment,
intervention.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(20), С. 10906 - 10906
Опубликована: Окт. 10, 2024
Diabetic
kidney
disease
(DKD)
is
a
serious
microvascular
complication
of
type
2
diabetes
mellitus
(T2DM).
Despite
the
numerous
genetic
loci
that
have
been
associated
with
in
T2DM,
architecture
DKD
remains
unclear
until
today.
In
contrast
to
SERPINE1,
contribution
SERPINB2
has
not
examined
DKD.
Therefore,
we
conducted
first
association
study
elucidate
its
role
total,
involved
197
patients
DKD,
155
T2DM
without
complications
(diabetic
disease,
diabetic
retinopathy,
and
neuropathy),
246
healthy
controls.
The
generalized
odds
ratio
(ORG)
was
calculated
estimate
risk
on
development.
present
regarding
SNPs
(rs4941230,
rs3819335,
rs13381217,
rs6140)
did
reveal
any
significant
between
variants
Additional
studies
other
populations
are
necessary
further
investigate
this
gene
progression
development
