Kidney
disease
is
a
significant
health
problem
worldwide,
affecting
an
estimated
10%
of
the
global
population.
encompasses
diverse
group
disorders
that
vary
in
their
underlying
pathophysiology,
clinical
presentation,
and
outcomes.
These
include
acute
kidney
injury
(AKI),
chronic
(CKD),
glomerulonephritis,
nephrotic
syndrome,
polycystic
disease,
diabetic
many
others.
Despite
distinct
etiologies,
these
share
common
feature
immune
system
dysregulation
metabolic
disturbances.
The
pathways
are
intimately
connected
interact
to
modulate
pathogenesis
diseases.
responses
diseases
includes
complex
interplay
between
various
cell
types,
including
resident
infiltrating
cells,
cytokines,
chemokines,
complement
factors.
factors
can
trigger
perpetuate
inflammation,
causing
renal
tissue
progressive
fibrosis.
In
addition,
play
critical
roles
diseases,
glucose
lipid
metabolism,
oxidative
stress,
mitochondrial
dysfunction,
altered
nutrient
sensing.
Dysregulation
contributes
progression
by
inducing
tubular
injury,
apoptosis,
Recent
studies
have
provided
insights
into
intricate
revealing
novel
therapeutic
targets
for
prevention
treatment
Potential
strategies
modulating
through
targeting
key
or
inhibiting
pro-inflammatory
signaling
pathways,
improving
function,
nutrient-sensing
such
as
mTOR,
AMPK,
SIRT1.
This
review
highlights
importance
potential
implications
pathways.
Physiological Reviews,
Journal Year:
2023,
Volume and Issue:
103(4), P. 2847 - 2892
Published: July 13, 2023
The
kidneys
play
a
key
role
in
maintaining
total
body
homeostasis.
complexity
of
this
task
is
reflected
the
unique
architecture
organ.
Ureteral
obstruction
greatly
affects
renal
physiology
by
altering
hemodynamics,
changing
glomerular
filtration
and
metabolism,
inducing
architectural
malformations
kidney
parenchyma,
most
importantly
fibrosis.
Persisting
pathological
changes
lead
to
chronic
disease,
which
currently
∼10%
global
population
one
major
causes
death
worldwide.
Studies
on
consequences
ureteral
date
back
1800s.
Even
today,
experimental
unilateral
(UUO)
remains
standard
model
for
tubulointerstitial
However,
has
certain
limitations
when
it
comes
studying
tubular
injury
repair,
as
well
limited
potential
human
translation.
Nevertheless,
provided
scientific
community
with
wealth
knowledge
(patho)physiology.
With
introduction
advanced
omics
techniques,
classical
UUO
remained
relevant
day
been
instrumental
understanding
fibrosis
at
molecular,
genomic,
cellular
levels.
This
review
details
concepts
recent
advances
obstructive
nephropathy,
highlighting
pathophysiological
hallmarks
responsible
functional
induced
obstruction,
special
emphasis
Cell Death Discovery,
Journal Year:
2024,
Volume and Issue:
10(1)
Published: May 13, 2024
Abstract
Macrophages
are
exceptionally
diversified
cell
types
and
perform
unique
features
functions
when
exposed
to
different
stimuli
within
the
specific
microenvironment
of
various
kidney
diseases.
In
instances
tissue
necrosis
or
infection,
patterns
associated
with
damage
pathogens
prompt
development
pro-inflammatory
macrophages
(M1).
These
M1
contribute
exacerbating
damage,
inflammation,
eventual
fibrosis.
Conversely,
anti-inflammatory
(M2)
arise
in
same
circumstances,
contributing
repair
regeneration
processes.
Impaired
causes
fibrosis,
hence
play
a
protective
pathogenic
role.
response
harmful
body,
inflammasomes,
complex
assemblies
multiple
proteins,
assume
pivotal
function
innate
immunity.
The
initiation
inflammasomes
triggers
activation
caspase
1,
which
turn
facilitates
maturation
cytokines,
death.
kidneys
possess
complete
elements
NLRP3
inflammasome,
including
NLRP3,
ASC,
pro-caspase-1.
When
activated,
it
caspase-1,
resulting
release
mature
proinflammatory
cytokines
(IL)-1β
IL-18
cleavage
Gasdermin
D
(GSDMD).
This
process
therefore
then
induces
pyroptosis,
leading
renal
death,
dysfunction.
NLRP3–ASC–caspase-1–IL-1β–IL-18
pathway
has
been
identified
as
factor
pathophysiology
numerous
this
review,
we
explore
current
progress
understanding
macrophage
behavior
concerning
injury,
fibrosis
kidneys.
Emphasizing
role
activated
both
advancement
recovery
phases
diseases,
article
delves
into
potential
strategies
modify
functionality
also
discusses
emerging
approaches
selectively
target
their
signaling
components
kidney,
aiming
facilitate
healing
Cells,
Journal Year:
2023,
Volume and Issue:
12(12), P. 1584 - 1584
Published: June 8, 2023
Kidney
disease
is
a
significant
health
problem
worldwide,
affecting
an
estimated
10%
of
the
global
population.
encompasses
diverse
group
disorders
that
vary
in
their
underlying
pathophysiology,
clinical
presentation,
and
outcomes.
These
include
acute
kidney
injury
(AKI),
chronic
(CKD),
glomerulonephritis,
nephrotic
syndrome,
polycystic
disease,
diabetic
many
others.
Despite
distinct
etiologies,
these
share
common
feature
immune
system
dysregulation
metabolic
disturbances.
The
pathways
are
intimately
connected
interact
to
modulate
pathogenesis
diseases.
responses
diseases
includes
complex
interplay
between
various
cell
types,
including
resident
infiltrating
cells,
cytokines,
chemokines,
complement
factors.
factors
can
trigger
perpetuate
inflammation,
causing
renal
tissue
progressive
fibrosis.
In
addition,
play
critical
roles
diseases,
glucose
lipid
metabolism,
oxidative
stress,
mitochondrial
dysfunction,
altered
nutrient
sensing.
Dysregulation
contributes
progression
by
inducing
tubular
injury,
apoptosis,
Recent
studies
have
provided
insights
into
intricate
revealing
novel
therapeutic
targets
for
prevention
treatment
Potential
strategies
modulating
through
targeting
key
or
inhibiting
pro-inflammatory
signaling
pathways,
improving
function,
nutrient-sensing
such
as
mTOR,
AMPK,
SIRT1.
This
review
highlights
importance
potential
implications
pathways.
Journal of Biochemical and Molecular Toxicology,
Journal Year:
2025,
Volume and Issue:
39(3)
Published: March 1, 2025
Sunitinib
(SUN)
is
a
chemotherapeutic
agent
showing
renal
toxicity
that
limits
its
clinical
applications.
The
present
research
aimed
to
clarify
the
potential
ameliorative
effects
of
secukinumab
(SEC)
and
dapagliflozin
(DAPA)
against
SUN-induced
underpinning
molecular
mechanisms.
For
this
purpose,
adult
Wistar
albino
rats
were
received
SUN
(25
mg/kg
3
times/week,
po)
co-treated
with
SEC
(3
mg/kg/every
2
weeks,
subcutaneously)
or
DAPA
(10
mg/kg/day,
for
4
weeks
compared
age-matched
control
group
(CON).
Markers
kidney
functions
assessed
in
serum
samples.
Kidneys
harvested
biochemical
histological
examination.
Compared
CON
group,
SUN-treated
displayed
signs
dysfunction
along
changes
ameliorated
by
DAPA.
Both
drugs
significantly
lowered
levels
IL-17,
but
exerted
more
inhibitory
effect
than
Additionally,
SUN-subjected
showed
significant
increases
expression
NLRP3
inflammasome
other
inflammatory
mediators
including
IL-1β,
END-1,
MCP-1.
This
was
associated
marked
decline
beclin-1.
Co-treatment
suppressed
NLRP3-induced
inflammation
while
enhanced
beclin-1-mediated
autophagy.
modulatory
on
beclin-1
superior
SEC.
Moreover,
both
similarly
attenuated
cleaved
caspase-3
interstitial
fibrosis
tissue
rats.
Collectively,
these
findings
may
repurpose
as
candidate
therapies
alleviate
rescue
functionality
cancer
cases.
Frontiers in Physiology,
Journal Year:
2025,
Volume and Issue:
16
Published: April 9, 2025
This
study
aims
to
systematically
review
the
risk
factors
for
major
adverse
cardiovascular
events
(MACE)
in
patients
with
coronary
heart
disease
who
have
undergone
percutaneous
intervention
(PCI).
Systematic
and
meta-analysis.
The
Cochrane
Library,
PubMed,
Web
of
Science,
China
National
Knowledge
Infrastructure
(CNKI),
Wanfang
Database,
VIP
Database
Chinese
Technical
Periodicals
(VIP)
were
screened
until
December
2024.
Case-control
studies
or
cohort
on
MACE
underwent
PCI.
Data
extraction
synthesis:
literature
review,
data
extraction,
quality
evaluation
conducted
by
two
independent
researchers,
meta-analysis
was
performed
using
RevMan
5.4
software.
main
outcome
that
occurred
during
follow-up
period.
A
total
40
articles
included.
erevealed
dyslipidemia
(OR
=
1.50;
95%
CI
[1.19,
1.89],
p
0.0007),
diabetes
mellitus
1.70;
[1.43,
2.02],
<
0.00001),
hypertension
1.62;
[1.35,
1.96],
0.0001),
history
smoking
2.08;
[1.51,
2.85],
poorer
ventricular
function
2.39;
[2.17-2.64],
impaired
left
ejection
fraction
(LVEF)
1.86;
[1.71-2.03],
door
balloon
(D-to-B)
time
0.61;
[0.42-0.88];
0.009),
thrombolysis
myocardial
infarction
(TIMI)
1.41;
[1.17,
1.70],
0.0004),
renal
dysfunction
1.82;
[1.37,
2.43],
multi-vessel
artery
0.41;
[0.37,
0.46],
0.0001)
significantly
associated
after
PCI
are
dyslipidemia,
hypertension,
mellitus,
history,
Killip
class
>
II,
LVEF
≤40%,
D-to-B
>90
min,
TIMI
flow
grade
≤
insufficiency,
multivessel
disease.