Kidney & Blood Pressure Research,
Год журнала:
2024,
Номер
49(1), С. 946 - 960
Опубликована: Окт. 18, 2024
Introduction:
Acute
kidney
injury
(AKI)
is
a
prevalent
renal
disorder.
The
occurrence
of
AKI
may
promote
the
formation
calcium
oxalate
stones
by
exerting
continuous
effects
on
tubular
epithelial
cells
(TECs).
We
aimed
to
delineate
molecular
interplay
between
and
nephrolithiasis.
Methods:
A
mild
(20
min)
severe
(30
ischemia-reperfusion
model
was
established
in
mice.
Seven
days
after
injury,
were
induced
using
glyoxylate
(Gly)
evaluate
impact
stones.
Transcriptome
sequencing
performed
TECs
elucidate
relationship
severity
Key
transcription
factors
(TFs)
regulating
differential
gene
levels
identified
motif
analysis,
pioglitazone,
ginkgetin,
fludarabine
used
for
targeted
therapy
validate
key
TFs
as
potential
targets
stone
treatment.
Results:
Severe
led
increased
deposition
crystals
renal,
impaired
function,
upregulation
stone-related
expression.
In
contrast,
associated
with
decreased
crystal
deposition,
preserved
downregulation
similar
Transcriptomic
analysis
revealed
that
genes
inflammation
cell
adhesion
pathways
significantly
upregulated
AKI,
while
related
energy
metabolism
AKI.
An
integrative
bioinformatic
uncovered
TF
regulatory
network
within
TECs,
pinpointing
PKNOX1
involved
inflammation-related
inhibiting
function
pioglitazone
could
simultaneously
reduce
increase
kidney.
On
other
hand,
also
protective
role
STAT1
kidneys
enhancing
ginkgetin
formation,
specific
inhibitor
STAT1,
fludarabine,
eliminate
therapeutic
Conclusion:
Inadequate
repair
increases
risk
regulated
playing
this
process.
Inhibiting
can
formation.
Conversely,
effective
through
expression
protect
TEC
activating
achieve
goal
treating
International Journal of Molecular Medicine,
Год журнала:
2024,
Номер
53(6)
Опубликована: Апрель 22, 2024
Urolithiasis
is
a
high‑incidence
disease
caused
by
calcium
oxalate
(mainly),
uric
acid,
phosphate,
struvite,
apatite,
cystine
and
other
stones.
The
development
of
kidney
stones
closely
related
to
renal
tubule
cell
damage
crystal
adhesion
aggregation.
Cell
death,
comprising
the
core
steps
damage,
can
be
classified
into
various
types
(i.e.,
apoptosis,
ferroptosis,
necroptosis
pyroptosis).
Different
types,
concentrations,
morphologies
sizes
cause
tubular
via
regulation
different
forms
death.
Oxidative
stress
high
or
concentrations
considered
precursor
variety
In
addition,
complex
crosstalk
exists
among
numerous
signaling
pathways
their
key
molecules
in
metabolic
disorder,
tricarboxylic
acid
cycle‑related
molecules,
such
as
citrate
succinate,
are
death
inhibition
stone
development.
However,
literature
review
associations
between
development,
metabolism
currently
lacking,
at
least
best
our
knowledge.
Thus,
present
summarizes
major
advances
understanding
regulated
urolithiasis
progression.
Advanced Science,
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 21, 2025
Abstract
The
initiation
of
calcium
oxalate
(CaOx)
kidney
stone
formation
is
highly
likely
to
stem
from
injury
the
renal
tubular
epithelial
cells
(RTECs)
induced
by
stimulation
an
aberrant
urinary
environment.
CHAC1
plays
a
critical
role
in
stress
response
mechanisms
regulating
glutathione
metabolism.
Endoplasmic
reticulum
(ER)
and
ferroptosis
are
demonstrated
be
involved
formation.
This
study
attempted
elucidate
mechanism
ER
stress‐dependent
CaOx
stones.
Here,
expression
performed
vivo
vitro
models.
These
findings
indicated
that
4‐Phenylbutyric
acid
(4‐PBA)treatment
deficiency
alleviated
ferroptotic
status,
including
restoring
GSH
content,
suppressing
Fe
2+
lipid
peroxidation
accumulation,
as
well
ferroptosis‐related
proteins.
Notably,
4‐PBA
treatment
both
attenuated
oxidative
damage,
improved
function,
importantly,
decreased
crystal
deposition.
Additionally,
ChIP‐seq
ChIP‐qPCR
analyses
vital
downstream
target
gene
ATF4.
results
ATF4
depletion
inhibited
upregulation
pro‐ferroptotic
Ox
stimulation.
Overall,
ATF4/CHAC1
axis
mediating
may
promising
research
direction
for
identifying
potential
strategy
prevent
treat
Scientific Reports,
Год журнала:
2025,
Номер
15(1)
Опубликована: Фев. 20, 2025
Schisandrin
B
(Sch
B)
derived
from
Schisandra
chinensis,
is
known
for
its
anti-inflammatory
and
anti-microbial
properties.
The
study
aimed
to
explore
Sch
B's
protective
roles
underlying
mechanisms
in
angiotensin
II
(Ang
II)
-
induced
ferroptosis,
atrial
fibrosis,
AF
using
both
vivo
vitro
models.
mice
model
generated
by
Ang
established
an
the
HL-1
cell
line
II.
We
assessed
fibrosis
through
histological
analysis
oxidative
stress
analysis.
employed
RT-qPCR
Western
blot
techniques
evaluate
mRNA
protein
expression.
significantly
attenuated
II-induced
development,
apoptosis,
myocardial
injury-related
molecules,
including
CK-MB
LDH.
Relative
DHE
intensity,
MDA,
NOX2,
NOX4
increased
significantly,
SOD
CAT
levels
decreased
markedly
mice.
treatment
could
inhibit
ROS
production
II-infused
In
addition,
showed
cardioprotective
effects
cells.
reduced
pro-inflammatory
cytokines,
IL-1β,
TNF-α,
IL-6,
restored
EX527
(SIRT1
inhibitor).
inhibited
intracellular
generation
cells,
which
were
Ex-527.
Furthermore,
increase
Fe2
+
concentration
caused
infusion,
was
recovered
expression
of
SIRT1,
SLC7A11,
GPX4
FTH1
while
reducing
patterns
Ex-527
treatment.
Our
experimental
data
suggest
that
protects
against
activating
SIRT1
vitro.
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease,
Год журнала:
2025,
Номер
unknown, С. 167791 - 167791
Опубликована: Март 1, 2025
Kidney
stones
represent
a
highly
prevalent
urological
disorder
worldwide,
with
high
incidence
and
recurrence
rates.
Calcium
oxalate
(CaOx)
crystal-induced
kidney
injury
serves
as
the
foundational
mechanism
for
formation
progression
of
CaOx
stones.
Regulated
cell
death
(RCD)
such
ferroptosis,
necroptosis,
pyroptosis
are
essential
in
pathophysiological
process
injury.
Ferroptosis,
newly
discovered
RCD,
is
characterized
by
its
reliance
on
iron-mediated
lipid
peroxidation.
Necroptosis,
widely
studied
programmed
necrosis,
initiates
necrotic
phenotype
that
resembles
apoptosis
appearance.
Pyroptosis,
type
RCD
involves
gasdermin
protein,
accompanied
inflammation
immune
response.
In
recent
years,
increasing
amounts
evidence
has
demonstrated
significant
processes
involved
Herein,
we
summed
up
roles
Furthermore,
delved
into
curative
potential
targeting
