Podocyte Death in Diabetic Kidney Disease: Potential Molecular Mechanisms and Therapeutic Targets
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(16), С. 9035 - 9035
Опубликована: Авг. 20, 2024
Cell
deaths
maintain
the
normal
function
of
tissues
and
organs.
In
pathological
conditions,
abnormal
activation
or
disruption
cell
death
often
leads
to
pathophysiological
effects.
Diabetic
kidney
disease
(DKD),
a
significant
microvascular
complication
diabetes,
is
linked
high
mortality
morbidity
rates,
imposing
substantial
burden
on
global
healthcare
systems
economies.
Loss
detachment
podocytes
are
key
changes
in
progression
DKD.
This
review
explores
potential
mechanisms
apoptosis,
necrosis,
autophagy,
pyroptosis,
ferroptosis,
cuproptosis,
podoptosis
podocytes,
focusing
how
different
modes
contribute
It
recognizes
limitations
current
research
presents
latest
basic
clinical
studies
targeting
podocyte
pathways
Lastly,
it
focuses
future
treat
DKD,
with
intention
inspiring
further
development
therapeutic
strategies.
Язык: Английский
Targeting programmed cell death in diabetic kidney disease: from molecular mechanisms to pharmacotherapy
Molecular Medicine,
Год журнала:
2024,
Номер
30(1)
Опубликована: Дек. 20, 2024
Abstract
Diabetic
kidney
disease
(DKD),
one
of
the
most
prevalent
microvascular
complications
diabetes,
arises
from
dysregulated
glucose
and
lipid
metabolism
induced
by
hyperglycemia,
resulting
in
deterioration
renal
cells
such
as
podocytes
tubular
epithelial
cells.
Programmed
cell
death
(PCD),
comprising
apoptosis,
autophagy,
ferroptosis,
pyroptosis,
necroptosis,
represents
a
spectrum
demise
processes
intricately
governed
genetic
mechanisms
vivo.
Under
physiological
conditions,
PCD
facilitates
turnover
cellular
populations
serves
protective
mechanism
to
eliminate
impaired
or
cells,
thereby
preserving
tissue
homeostasis
amidst
hyperglycemic
stress.
However,
existing
research
predominantly
elucidates
individual
modes
death,
neglecting
intricate
interplay
mutual
modulation
observed
among
various
forms
PCD.
In
this
comprehensive
review,
we
delineate
diverse
regulatory
governing
elucidate
crosstalk
dynamics
distinct
pathways.
Furthermore,
review
recent
advancements
understanding
pathogenesis
explore
their
implications
DKD.
Additionally,
potential
natural
products
derived
primarily
botanical
sources
therapeutic
agents,
highlighting
multifaceted
effects
on
modulating
crosstalk,
proposing
novel
strategies
for
DKD
treatment.
Язык: Английский
Tanshinone IIA Promotes Ferroptosis in cutaneous Melanoma via STAT1-Mediated Upregulation of PTGS2 Expression
Phytomedicine,
Год журнала:
2025,
Номер
unknown, С. 156702 - 156702
Опубликована: Апрель 1, 2025
Язык: Английский
Calcium/Calmodulin-Dependent Protein Kinase II β Regulates Autophagy Dependent Ferroptosis of Neurons after Cerebral Ischemic Injury by Activating the AREG/JUN/ELAVL1 Pathway
Neurochemical Research,
Год журнала:
2025,
Номер
50(2)
Опубликована: Апрель 1, 2025
Язык: Английский
Salvia miltiorrhiza -derived exosome-like nanoparticles improve diabetic cardiomyopathy by inhibiting NLRP3 inflammasome-mediated macrophage pyroptosis via targeting the NEDD4/SGK1 axis
Nanomedicine,
Год журнала:
2025,
Номер
unknown, С. 1 - 12
Опубликована: Май 20, 2025
Exosome-like
nanoparticles
mediate
intercellular
communication
and
regulate
gene
expression.
In
this
study,
we
isolated
purified
exosome-like
from
Salvia
miltiorrhiza
(SM-ELNs),
a
traditional
Chinese
medicinal
herb,
investigated
their
therapeutic
effects
on
diabetic
cardiomyopathy
(DCM).
To
investigate
the
effect
of
SM-ELNs
DCM,
established
mouse
model
via
HFD/STZ
treatment.
Cardiac
function
was
assessed
by
echocardiography.
hypertrophy
measuring
heart
weight/body
weight
ratio
HE
staining,
while
myocardial
fibrosis
evaluated
using
Masson's
trichrome
staining.
The
role
NLRP3
inflammasome
inhibition
macrophage
pyroptosis
were
both
in
vivo
vitro.
interaction
between
NEDD4
SGK1
analyzed
Co-IP
ubiquitination
assays.
treatment
alleviated
cardiac
histopathological
changes
DCM
mice.
Moreover,
suppressed
activation
subsequent
vitro
models.
Mechanistically,
facilitated
degradation
macrophages.
Both
depletion
addition
could
counteract
SM-ELNs-induced
suppression
inflammasome-triggered
LPS/ATP-treated
RAW264.7
cells.
Our
study
provides
first
evidence
that
inhibit
inflammasome-mediated
modulating
NEDD4/SGK1
axis.
Язык: Английский
ELAVL1 promotes ferroptosis via the TRIM21/HOXD8 axis to inhibit osteogenic differentiation in congenital pseudoarticular tibia‐derived mesenchymal stem cells
Journal of Cell Communication and Signaling,
Год журнала:
2025,
Номер
19(2)
Опубликована: Май 21, 2025
Язык: Английский
Therapeutic effects of natural compounds against diabetic complications via targeted modulation of ferroptosis
Frontiers in Pharmacology,
Год журнала:
2024,
Номер
15
Опубликована: Сен. 18, 2024
Diabetes
mellitus,
a
chronic
metabolic
disorder,
can
result
in
serious
tissue
and
organ
damage
due
to
long-term
dysfunction,
leading
various
complications.
Therefore,
exploring
the
pathogenesis
of
diabetic
complications
developing
effective
prevention
treatment
drugs
is
crucial.
The
role
ferroptosis
has
emerged
as
significant
area
research
recent
years.
Ferroptosis,
recently
discovered
form
regulated
cell
death
closely
linked
iron
metabolism
imbalance
lipid
peroxidation,
garnered
increasing
attention
studies
potential
natural
products
its
regulation.
This
review
provides
an
overview
mechanisms
underlying
ferroptosis,
outlines
detection
methods,
synthesizes
information
from
product
databases.
It
also
summarizes
current
on
how
may
regulate
Studies
have
shown
that
these
modulate
process
by
influencing
ion
balance
combating
oxidative
stress.
highlights
treating
regulating
offering
new
strategy
for
managing
such
Язык: Английский
Autophagy Regulates Ferroptosis‐Mediated Diabetic Liver Injury by Modulating the Degradation of ACSL4
Journal of Diabetes Research,
Год журнала:
2024,
Номер
2024(1)
Опубликована: Янв. 1, 2024
Diabetic
liver
injury
is
a
serious
complication
due
to
the
lack
of
effective
treatments
and
unclear
pathogenesis.
Ferroptosis,
form
cell
death
involving
reactive
oxygen
species
(ROS)-dependent
lipid
peroxidation
(LPO),
closely
linked
autophagy
diabetic
complications.
Therefore,
this
study
aimed
at
investigating
role
in
regulating
ferroptosis
by
modulating
degradation
acyl-CoA
synthetase
long-chain
family
member
4
(ACSL4)
hepatocytes
its
potential
impact
on
injury.
Язык: Английский