Clinical Kidney Journal,
Год журнала:
2024,
Номер
17(8)
Опубликована: Июль 10, 2024
Many
kidney
diseases
are
associated
with
proteinuria.
Since
proteinuria
is
independently
function
loss,
anti-proteinuric
medication,
often
in
combination
dietary
salt
restriction,
comprises
a
major
cornerstone
the
prevention
of
progressive
failure.
Nevertheless,
complete
remission
very
difficult
to
achieve,
and
most
patients
persistent
slowly
progress
toward
It
well-recognized
that
leads
inflammation
fibrosis
via
various
mechanisms.
Among
others,
complement
activation
at
apical
side
proximal
tubular
epithelial
cells
suggested
play
crucial
role
as
cause
loss
function.
However,
hitherto
limited
attention
given
pathophysiological
relative
glomerular
activation.
This
review
aims
summarize
evidence
for
proteinuric
relation
Nutrients,
Год журнала:
2025,
Номер
17(5), С. 758 - 758
Опубликована: Фев. 21, 2025
Advanced
glycation
end
products
(AGEs)
represent
a
class
of
toxic
and
irreversible
compounds
formed
through
non-enzymatic
reactions
between
proteins
or
lipids
carbonyl
compounds.
AGEs
can
arise
endogenously
under
normal
metabolic
conditions
in
pathological
states
such
as
diabetes,
kidney
disease,
inflammatory
disorders.
Additionally,
they
be
obtained
exogenously
dietary
intake,
particularly
from
foods
high
fat
sugar,
well
grilled
processed
items.
accumulate
various
organs
have
been
increasingly
recognized
significant
contributors
to
the
progression
numerous
diseases,
disease.
As
plays
crucial
role
AGE
metabolism
excretion,
it
is
highly
susceptible
AGE-induced
damage.
In
this
review,
we
provide
comprehensive
discussion
on
onset
including
diabetic
nephropathy,
chronic
acute
injury.
We
explore
potential
biological
mechanisms
involved,
accumulation,
AGEs-RAGE
axis,
oxidative
stress,
inflammation,
gut
microbiota
dysbiosis,
DNA
Furthermore,
discuss
recent
findings
characteristics
vivo
their
pathogenic
impact
renal
function.
examine
clinical
significance
early
diagnosis,
treatment,
prognosis
highlighting
biomarkers
therapeutic
targets.
By
integrating
advancements
research,
review
aims
new
insights
strategies
for
mitigating
AGE-related
damage
improving
disease
management.
Clinical and Translational Medicine,
Год журнала:
2025,
Номер
15(3)
Опубликована: Фев. 25, 2025
Abstract
Background
Macrophages
have
been
shown
to
contribute
renal
injury
and
fibrosis
as
well
repair.
Recently,
Triggering
Receptor
Expressed
on
Myeloid
Cells
2
(TREM2)‐positive
macrophages
play
important
roles
in
regulating
tissue
inflammation
However,
it
remains
unclear
whether
they
can
mitigate
the
transition
from
acute
kidney
chronic
disease
(the
AKI–CKD
transition).
Methods
The
was
generated
by
unilateral
ischaemia–reperfusion
(UIRI)
wild‐type
(WT)
Trem2
knockout
mice.
F4/80
magnetic
beads
were
used
isolate
macrophages.
Flow
cytometry
determine
levels
of
TREM2
CD11b
levels.
Quantitative
reverse
transcription
polymerase
chain
reaction
(qRT‐PCR),
Western
blotting
histological
staining
performed
expression
cytokines
fibrotic
markers.
RNA‐seq
investigate
transcriptomic
changes
between
WT
bone
marrow‐derived
(BMDMs).
TREM2‐overexpressing
using
lentivirus
transferred
intravenously
UIRI
Results
exhibited
a
strong
protective
effect
transition.
Genetic
deletion
resulted
increased
exacerbated
Interestingly,
we
found
that
hypoxia
could
increase
via
HIF‐1α.
Upregulated
enhanced
macrophage
phagocytosis
suppressed
pro‐inflammatory
cytokines,
resulting
lower
apoptosis
tubular
epithelial
cells.
Using
analysis,
showed
regulatory
effects
orchestrated
PI3K‐AKT
pathway.
Pharmacological
regulation
pathway
modulate
macrophage‐mediated
phagocytosis.
In
addition,
an
adoptive
cell
therapy
effectively
reduced
immune
infiltration,
Conclusion
Our
study
not
only
provides
valuable
mechanistic
insights
into
role
but
also
offers
new
avenue
for
macrophage‐based
treat
diseases.
Key
points
worsens
accelerates
is
upregulated
HIF1α
An
reduces
fibrosis.
Research Square (Research Square),
Год журнала:
2025,
Номер
unknown
Опубликована: Март 31, 2025
AbstractPurpose
Acute
kidney
injury
(AKI)
is
a
common
clinical
complication
of
cardiac
surgeries.
Although
urinary
particle
analysis
useful
for
differentiating
AKI,
its
value
in
AKI
diagnosis
has
not
yet
been
well
described.
We
sought
to
determine
the
contribution
AKI.
Methods
Two-hundred
and
thirty-nine
adult
patients
were
prospectively
included
after
surgery.
The
diagnostic
performance
at
different
time
points
intensive
care
unit
(ICU)
admission
was
evaluated.
diagnosed
classified
according
KDIGO
definitions.
Urinary
particles,
including
renal
tubular
epithelial
cells
(RTEC)
non-hyaline
casts,
Nephrocheck®,
alpha-1-microglobulin
γ-glutamyltransferase
(GGT)
levels
measured
4,
12
24h
ICU
evaluated
against
endpoints.
Results
Of
239
included,
41
(17.1%)
had
stage
1,
118
(49.2%)
2,
16
(6.7%)
3.
In
early
postoperative
period,
Nephrocheck®
good
predictors
≥1
within
48h
(primary
endpoint)
≥2
(1st
secondary
endpoint),
respectively.
Furthermore,
12h
admission,
RTEC
highest
predictive
up
based
on
serum
creatinine
alone
all
criteria
7d
admission.
Correction
obtained
counts
hydration
status
did
improve
results.
Conclusion
with
following
surgery,
especially
Scientific Reports,
Год журнала:
2025,
Номер
15(1)
Опубликована: Фев. 7, 2025
Ischemia-reperfusion
injury
(IRI)
is
one
of
the
leading
causes
acute
kidney
(AKI),
predisposing
patients
to
chronic
disease
(CKD)
due
maladaptive
renal
repair.
Nevertheless,
molecular
mechanisms
and
biomarkers
that
cause
repair
remain
unclear.
In
this
study,
we
used
single-nucleus
RNA
sequencing
data
from
GEO
database
(GSE139107)
identify
markers
during
transition
AKI
CKD
caused
by
IRI.
Analysis
intercellular
crosstalk,
trajectory
machine
learning
algorithms
revealed
hub
cell
clusters
genes.
Proximal
tubule
(PT)
cells,
especially
a
new
cluster
(New
PT2),
significantly
interacted
with
fibroblasts
transition.
The
expression
levels
genes
were
validated
using
bulk
RNA-seq
(GSE98622)
further
confirmed
through
RT-qPCR
immunohistochemical
analysis
in
ischemia-reperfusion
(uIRI)
mice.
Ankrd1,
gene
New
PT2,
showed
sustained
upregulation
proximal
AKI.
Compared
sham-operated
group,
Ankrd1
mice
increased
at
0.5
days
post-reperfusion,
peaked
day
1,
remained
elevated
up
60
days.
This
study
indicated
was
positively
associated
progression
may
potentially
serve
as
valuable
biomarker
for
transitional
process.
The Journal of Experimental Medicine,
Год журнала:
2025,
Номер
222(6)
Опубликована: Март 28, 2025
Maladaptive
repair
following
kidney
injury
leads
to
the
development
of
disease.
In
this
issue
JEM,
Ajay
et
al.
(https://doi.org/10.1084/jem.20231107)
uncover
role
breast
cancer
susceptibility
gene
1
(BRCA1)
in
cell
cycle
arrest,
DNA
damage,
and
senescence,
preventing
maladaptive
repair.
Biomedicine & Pharmacotherapy,
Год журнала:
2024,
Номер
178, С. 117210 - 117210
Опубликована: Июль 25, 2024
The
ubiquitin-proteasome
system
(UPS)
is
a
basic
regulatory
mechanism
in
cells
that
essential
for
maintaining
cell
homeostasis,
stimulating
signal
transduction,
and
determining
fate.
These
biological
processes
require
coordinated
signaling
cascades
across
members
of
the
UPS
to
achieve
substrate
ubiquitination
deubiquitination.
role
fibrotic
diseases
has
attracted
widespread
attention,
aberrant
expression
affects
fibrosis
process.
In
this
review,
we
provide
an
overview
its
relevance
diseases.
Moreover,
first
time,
explore
detail
how
promotes
or
inhibits
renal
by
regulating
such
as
pathways,
inflammation,
oxidative
stress,
cycle,
emphasizing
status
fibrosis.
Further
research
on
may
reveal
new
strategies
preventing
