Frontiers in Medicine,
Journal Year:
2024,
Volume and Issue:
11
Published: Dec. 3, 2024
Background
and
aims
The
immune
system
plays
a
crucial
role
in
the
development
of
kidney
diseases.
Chronic
disease
(CKD)
can
lead
to
various
complications,
potentially
affecting
multiple
systems
throughout
body.
Currently,
description
human
CKD
is
not
comprehensive
enough.
Constructing
atlas
using
single-cell
RNA
sequencing
(scRNA-seq)
provide
deeper
insights
into
composition
functional
changes
cells
CKD,
facilitating
discovery
new
therapeutic
targets.
Methods
We
processed
integrated
scRNA-seq
datasets
from
healthy
kidneys
three
independent
cohorts
same
approach
(including
42
normal
samples
23
chronic
samples).
Subsequently,
we
conducted
gene
enrichment
intercellular
communication
analysis
construct
an
cell
patients.
Results
identified
nine
major
clusters.
Further
clustering
different
clusters
revealed
that,
compared
kidneys,
patients’
had
decreased
CD16+
NK
while
CD4+
naive
helper
T
CCR7+
DC
increased.
Partial
activation
WNT
signaling
pathway
was
observed
patients,
some
metabolism-related
genes
were
inhibited.
Myeloid
subgroups
also
exhibited
abnormal
alterations.
Additionally,
discovered
unique
population
SPP1
macrophages
which
are
recruited
by
chemokines
released
aPT
aTAL
subpopulations.
These
may
promote
cellular
fibrosis
through
SPP1,
FN1,
receptors.
Conclusion
established
as
type
CKD.
interaction
between
damaged
serve
potential
target
for
treating
future.
Kidney International,
Journal Year:
2024,
Volume and Issue:
106(1), P. 24 - 34
Published: April 16, 2024
Kidney
epithelial
cells
have
very
high
energy
requirements,
which
are
largely
met
by
fatty
acid
oxidation.
Complex
changes
in
lipid
metabolism
observed
patients
with
kidney
disease.
Defects
oxidation
and
increased
uptake,
especially
the
context
of
hyperlipidemia
proteinuria,
contribute
to
this
excess
build-up
exacerbate
disease
development.
Recent
studies
also
highlighted
role
de
novo
lipogenesis
fibrosis.
The
defect
causes
starvation.
Increased
synthesis,
lower
can
cause
toxic
build-up,
reactive
oxygen
species
generation,
mitochondrial
damage.
A
better
understanding
these
metabolic
processes
may
open
new
treatment
avenues
for
diseases
targeting
metabolism.
Lipids in Health and Disease,
Journal Year:
2025,
Volume and Issue:
24(1)
Published: Feb. 25, 2025
Elevated
incidence
of
metabolic
disorders
has
been
reported
worldwide
in
the
recent
decade,
highlighting
need
for
developing
efficient
therapies.
These
diseases
result
from
a
complex
interplay
various
factors
that
contribute
to
disease
progression,
complications,
and
resistance
current
treatment
options.
Acetyl-CoA
Synthetase
Short
Chain
Family
Member
2
(ACSS2)
is
nucleo-cytosolic
enzyme
with
both
lipogenic
regulatory
roles.
Studies
on
ACSS2
have
shown
it
involved
pathways
commonly
dysregulated
disorders,
leading
fat
deposition
disrupted
cellular
signaling.
Although
multiple
studies
suggested
role
rewiring
during
tumorigenesis,
few
examined
its
involvement
pathophysiology
diseases.
Recent
evidence
indicates
may
pathogenesis
making
examination
great
interest
potentially
aiding
development
new
therapeutic
strategies.
The
objective
this
review
summarize
understanding
ACSS2's
potential
as
target.
FEBS Journal,
Journal Year:
2025,
Volume and Issue:
unknown
Published: March 25, 2025
The
tumor
microenvironment
(TME)
is
a
complex
ecosystem,
encompassing
variety
of
cellular
and
non-cellular
elements
surrounding
interacting
with
cancer
cells,
overall
promoting
growth,
immune
evasion,
therapy
resistance.
In
the
context
solid
tumors,
factors,
such
as
hypoxia,
nutritional
competition,
increased
stress
responses,
glucose
demand,
PD-1
signals
strongly
influence
metabolic
alterations
in
TME,
highly
contributing
to
maintenance
tumor-supportive
immune-suppressive
milieu.
Cancer
cell-induced
partly
result
an
fatty
acid
(FA)
metabolism
within
which
favors
recruitment
M2
macrophages
myeloid-derived
suppressor
crucial
contributors
T-cell
exhaustion,
exclusion,
decreased
effector
functions.
drastic
pro-tumoral
changes
induced
by
rewiring
signaling
loops
that
support
progression
metastatic
spreading,
negatively
impact
efficacy.
As
tumor-
are
increasingly
gaining
attention
due
their
potential
therapeutic
implications,
we
discuss
effects
altered
lipid
on
progression,
response,
efficacy
lung
cancer.
particular,
focus
our
analysis
tumor-induced
experienced
T
lymphocytes
possible
strategies
overcome
immunotherapy
resistance
targeting
specific
pathways
cells.
Journal of Clinical Investigation,
Journal Year:
2024,
Volume and Issue:
134(4)
Published: Feb. 14, 2024
Ten
percent
of
the
population
worldwide
suffers
from
chronic
kidney
disease
(CKD),
but
mechanisms
driving
CKD
pathology
are
incompletely
understood.
While
dysregulated
lipid
metabolism
is
one
hallmark
CKD,
pathogenesis
cellular
accumulation
remains
unclear.
In
this
issue
JCI,
Mukhi
et
al.
Identify
acyl-CoA
synthetase
short-chain
family
2
(ACSS2)
as
a
risk
gene
and
demonstrate
role
for
ACSS2
in
de
novo
lipogenesis
(DNL).
Notably,
genetic
or
pharmacological
inhibition
DNL
protected
against
progression
mice.
These
findings
warrant
evaluation
with
respect
to
efficacy
safety
people
CKD.
Science Advances,
Journal Year:
2024,
Volume and Issue:
10(49)
Published: Dec. 4, 2024
Angiopoietin-like
4
(ANGPTL4),
a
key
protein
involved
in
lipoprotein
metabolism,
has
diverse
effects.
There
is
an
association
between
Angptl4
and
diabetic
kidney
disease;
however,
this
not
been
well
investigated.
We
show
that
both
podocyte-
tubule-specific
ANGPTL4
are
crucial
fibrogenic
molecules
diabetes.
Diabetes
accelerates
the
phenotype
control
mice
but
mutant
mice.
The
protective
effect
observed
correlated
with
reduction
stimulator
of
interferon
genes
pathway
activation,
expression
pro-inflammatory
cytokines,
reduced
epithelial-to-mesenchymal
transition
endothelial-to-mesenchymal
transition,
lessened
mitochondrial
damage,
increased
fatty
acid
oxidation.
Mechanistically,
we
demonstrate
or
tubule-secreted
interacts
Integrin
β1
influences
dipeptidyl-4
β1.
utility
targeted
pharmacologic
therapy
specifically
inhibits
gene
kidneys
protects
from
proteinuria
fibrosis.
Together,
these
data
tubule-derived
kidneys.
