Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: Dec. 10, 2024
Triple-negative
breast
cancer
(TNBC)
stands
as
the
most
complex
and
daunting
subtype
of
affecting
women
globally.
Regrettably,
treatment
options
for
TNBC
remain
limited
due
to
its
clinical
complexity.
However,
immunotherapy
has
emerged
a
promising
avenue,
showing
success
in
developing
effective
therapies
advanced
cases
improving
patient
outcomes.
Improving
treatments
involves
reducing
side
effects,
minimizing
systemic
toxicity,
enhancing
efficacy.
Unlike
traditional
immunotherapy,
engineered
nonmaterial's
can
precisely
target
TNBC,
facilitating
immune
cell
access,
antigen
presentation,
triggering
lasting
responses.
Nanocarriers
with
enhanced
sensitivity
specificity,
specific
cellular
absorption,
low
toxicity
are
gaining
attention.
Nanotechnology-driven
immunoengineering
strategies
focus
on
targeted
delivery
systems
using
multifunctional
molecules
precise
tracking,
diagnosis,
therapy
TNBC.
This
study
delves
into
TNBC's
tumour
microenvironment
(TME)
remodeling,
therapeutic
resistance,
nanotechnology.
Journal of Cellular Biochemistry,
Journal Year:
2024,
Volume and Issue:
125(10)
Published: Aug. 2, 2024
ABSTRACT
In
this
study,
we
investigate
the
effect
of
neuregulin
4
(NRG4)
on
podocyte
damage
in
a
mouse
model
diabetic
nephropathy
(DN)
and
elucidate
underlying
molecular
mechanisms.
vivo
experiments
were
conducted
using
C57BL/6
DN
to
determine
NRG4
proteinuria
injury,
vitro
performed
with
conditionally
immortalized
podocytes
treated
high
glucose
assess
protective
effects
injury.
Autophagy‐related
protein
levels
related
signaling
pathways
evaluated
both
vitro.
The
involvement
adenosine
monophosphate‐activated
kinase
(AMPK)/mammalian
target
rapamycin
(mTOR)
pathway
was
detected
chloroquine
or
AMPK
inhibitors.
results
showed
that
AMPK/mTOR
involved
roles
against
glucose‐mediated
Also,
significantly
decreased
albuminuria
mice.
PAS
staining
indicated
mitigated
glomerular
volume
mesangium
expansion
Consistently,
western
blot
RT‐PCR
analyses
confirmed
expression
pro‐fibrotic
molecules
glomeruli
immunofluorescence
retained
podocin
nephrin,
whereas
transmission
electron
microscopy
revealed
alleviated
mice,
apoptosis
increased
nephrin
podocin,
while
decreasing
desmin
HIF1α.
Overall,
improved
albuminuria,
glomerulosclerosis,
glomerulomegaly,
hypoxia
inhibited
HG‐induced
injury
apoptosis.
Furthermore,
autophagy
but
reactivated
following
intervention.
intervention
found
partially
activate
via
pathway.
Consequently,
when
suppressed
inhibited,
beneficial
diminished.
These
indicate
attenuates
by
promoting
kidneys
part,
activating
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(2), P. 790 - 790
Published: Jan. 8, 2024
Diabetic
kidney
disease
(DKD),
as
a
major
microvascular
complication
of
both
type
1
and
2
diabetes
mellitus
(DM),
accounts
for
over
40%
patients
that
reach
end-stage
renal
are
referred
to
replacement
therapies
[...]
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(16), P. 9035 - 9035
Published: Aug. 20, 2024
Cell
deaths
maintain
the
normal
function
of
tissues
and
organs.
In
pathological
conditions,
abnormal
activation
or
disruption
cell
death
often
leads
to
pathophysiological
effects.
Diabetic
kidney
disease
(DKD),
a
significant
microvascular
complication
diabetes,
is
linked
high
mortality
morbidity
rates,
imposing
substantial
burden
on
global
healthcare
systems
economies.
Loss
detachment
podocytes
are
key
changes
in
progression
DKD.
This
review
explores
potential
mechanisms
apoptosis,
necrosis,
autophagy,
pyroptosis,
ferroptosis,
cuproptosis,
podoptosis
podocytes,
focusing
how
different
modes
contribute
It
recognizes
limitations
current
research
presents
latest
basic
clinical
studies
targeting
podocyte
pathways
Lastly,
it
focuses
future
treat
DKD,
with
intention
inspiring
further
development
therapeutic
strategies.
Frontiers in Genetics,
Journal Year:
2023,
Volume and Issue:
14
Published: Nov. 6, 2023
Background:
Diabetic
nephropathy
(DN)
is
the
most
common
complication
of
diabetes,
and
its
pathogenesis
complex
involving
a
variety
programmed
cell
death,
inflammatory
responses,
autophagy
mechanisms.
Disulfidptosis
newly
discovered
mechanism
death.
There
are
little
studies
about
role
disulfidptosis
on
DN.
Methods:
First,
we
obtained
data
required
for
this
study
from
GeneCards
database,
Nephroseq
v5
GEO
database.
Through
differential
analysis,
disulfidptosis-related
genes.
At
same
time,
through
WGCNA
key
module
genes
in
DN
patients.
The
intersecting
were
further
screened
by
Lasso
as
well
SVM-RFE.
By
results
two,
ended
up
with
gene
diabetic
nephropathy.
diagnostic
performance
expression
verified
GSE30528,
GSE30529,
GSE96804,
datasets.
Using
clinical
information
investigated
correlation
between
estimated
glomerular
filtration
rate
(eGFR)
serum
creatinine
content.
Next,
constructed
nomogram
analyzed
immune
microenvironment
patients
identification
subtypes
facilitates
individualized
treatment
Results:
We
91
39
Taking
intersection
preliminarily
20
characteristic
found
that
these
positively
correlated
each
other.
Further
screening
SVM-RFE
algorithms
identified
CXCL6,
CD48,
C1QB,
COL6A3
Clinical
analysis
levels
closely
related
to
eGFR.
Immune
infiltration
higher
samples
than
normal
samples.
Conclusion:
validated
4
may
be
promote
onset
eGFR
infiltrated
kidney
tissue.