Cell Death and Disease,
Год журнала:
2024,
Номер
15(12)
Опубликована: Дек. 18, 2024
Abstract
Acute
kidney
injury
(AKI)
is
a
significant
global
health
issue,
which
often
caused
by
cisplatin
therapy
and
characterized
mitochondrial
dysfunction.
Restoring
homeostasis
in
tubular
cells
could
exert
therapeutic
effects.
Here,
we
investigated
Slc25a21,
carrier,
as
potential
target
for
AKI
intervention.
Renal
Slc25a21
expression
negatively
associated
with
function
both
patients
cisplatin-induced
murine
models.
Sustaining
renal
of
slowed
down
progression
reducing
cellular
apoptosis,
necroptosis,
the
inflammatory
response,
likely
through
its
regulation
2-oxoadipate
conversion.
highly
expressed
proximal
epithelial
cells,
down-regulation
contributes
to
compromised
biogenesis
integrity,
well
impaired
oxidative
phosphorylation.
Mechanistically,
reduced
disrupts
transport,
affecting
related
metabolites
influx
tricarboxylic
acid
cycle.
These
findings
demonstrate
previously
unappreciated
metabolic
suggest
that
targeting
sustaining
be
novel
strategy
AKI.
Antioxidants,
Год журнала:
2024,
Номер
13(12), С. 1540 - 1540
Опубликована: Дек. 16, 2024
Obesity
has
emerged
as
a
significant
public
health
crisis,
closely
linked
to
the
pathogenesis
and
progression
of
chronic
kidney
disease
(CKD).
This
review
explores
intricate
relationship
between
obesity-induced
lipid
metabolism
disorders
renal
health.
We
discuss
how
excessive
free
fatty
acids
(FFAs)
lead
accumulation
in
tissues,
resulting
cellular
lipotoxicity,
oxidative
stress,
inflammation,
ultimately
contributing
injury.
Key
molecular
mechanisms,
including
roles
transcriptional
regulators
like
PPARs
SREBP-1,
are
examined
for
their
implications
dysregulation.
The
also
highlights
impact
glomerular
tubular
overload
on
pathology,
emphasizing
podocytes
cells
maintaining
function.
Various
therapeutic
strategies
targeting
metabolism,
pharmacological
agents
such
statins
SGLT2
inhibitors,
well
lifestyle
modifications,
discussed
potential
mitigate
CKD
obese
individuals.
Future
research
directions
suggested
better
understand
mechanisms
linking
develop
personalized
approaches.
Ultimately,
addressing
obesity-related
may
enhance
improve
outcomes
individuals
suffering
from
CKD.
Biology,
Год журнала:
2024,
Номер
13(9), С. 655 - 655
Опубликована: Авг. 24, 2024
Although
the
human
body
needs
nickel
as
a
trace
element,
too
much
exposure
can
be
hazardous.
The
effects
of
on
cells
include
inducing
oxidative
stress,
interfering
with
DNA
damage
repair,
and
altering
epigenetic
modifications.
Glucose
metabolism
lipid
are
closely
related
to
stress;
however,
their
role
in
nickel-induced
further
study.
In
Institute
Cancer
Research
(ICR)
mice,
our
findings
indicated
that
stress
increased
levels
blood
indicators
(triglycerides,
high-density
lipoprotein,
cholesterol)
by
about
50%,
glucose
more
than
two-fold,
glycated
serum
protein
nearly
20%.
At
same
time,
(malondialdehyde)
inflammation
(Interleukin
6)
30%
kidney.
Based
next-generation
sequencing
technology,
we
detected
analyzed
differentially
expressed
genes
kidney
caused
stress.
Bioinformatics
analysis
experimental
verification
showed
inhibited
expression
AMPK
PPAR
signaling
pathways.
finding
induces
injury
inhibits
key
involved
pathways
provides
theoretical
basis
for
deeper
understanding
mechanism
injury.
Current Opinion in Endocrinology Diabetes and Obesity,
Год журнала:
2024,
Номер
unknown
Опубликована: Ноя. 20, 2024
This
review
highlights
emerging
evidence
supporting
the
premise
of
precision
diabetes
care
including
but
not
limited
to
monogenic
and
discuss
potential
opportunities,
challenges,
limitations
for
clinical
adoption.
Cell Death and Disease,
Год журнала:
2024,
Номер
15(12)
Опубликована: Дек. 18, 2024
Abstract
Acute
kidney
injury
(AKI)
is
a
significant
global
health
issue,
which
often
caused
by
cisplatin
therapy
and
characterized
mitochondrial
dysfunction.
Restoring
homeostasis
in
tubular
cells
could
exert
therapeutic
effects.
Here,
we
investigated
Slc25a21,
carrier,
as
potential
target
for
AKI
intervention.
Renal
Slc25a21
expression
negatively
associated
with
function
both
patients
cisplatin-induced
murine
models.
Sustaining
renal
of
slowed
down
progression
reducing
cellular
apoptosis,
necroptosis,
the
inflammatory
response,
likely
through
its
regulation
2-oxoadipate
conversion.
highly
expressed
proximal
epithelial
cells,
down-regulation
contributes
to
compromised
biogenesis
integrity,
well
impaired
oxidative
phosphorylation.
Mechanistically,
reduced
disrupts
transport,
affecting
related
metabolites
influx
tricarboxylic
acid
cycle.
These
findings
demonstrate
previously
unappreciated
metabolic
suggest
that
targeting
sustaining
be
novel
strategy
AKI.
