Leveraging Immunogenic Cell Death to Enhance the Immune Response against Malignant Pleural Mesothelioma Tumors
Meng Rui Chang,
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Egor M. Matnurov,
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Chengnan Wu
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et al.
Journal of the American Chemical Society,
Journal Year:
2025,
Volume and Issue:
147(9), P. 7908 - 7920
Published: Feb. 24, 2025
Although
various
metal-based
compounds
have
exhibited
excellent
immunogenic
cell
death
(ICD)-inducing
properties
both
in
vitro
and
vivo,
the
majority
of
these
been
discovered
serendipitously.
In
this
work,
we
successfully
synthesized
characterized
35
cyclometalated
Au(III)
complexes
containing
dithiocarbamate
ligands,
with
25
being
previously
unreported.
Their
ability
to
induce
phagocytosis
against
immunologically
"cold"
malignant
pleural
mesothelioma
(MPM)
cells
was
strongly
dependent
on
scaffold
overall
lipophilicity
complexes.
We
elucidated
role
mechanisms
observed
ICD
effects
identified
correlations
between
necrotic
ICD,
vivo.
Complex
2G,
its
high
rates
low
necrosis
rates,
recognized
as
a
bona
fide
inducer,
demonstrating
remarkably
long-lasting
immune
response
vaccinated
mice.
contrast,
complex
1C,
by
failed
elicit
sustained
upon
following
vaccination;
however,
it
triggered
selective
activation
calreticulin
tumors
direct
vivo
administration.
Overall,
study
offers
framework
for
predicting
structurally
similar
complexes,
potential
extension
other
series
metal
Language: Английский
Exploring molecular disparities of H-type vasculature endothelial cells in osteonecrosis of the femoral head through single-cell analysis
Shi Wei,
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Dong Li,
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Qian Xu
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et al.
BMC Musculoskeletal Disorders,
Journal Year:
2025,
Volume and Issue:
26(1)
Published: Feb. 6, 2025
Recent
studies
highlight
the
role
of
H-type
vasculature
in
bone
regeneration.
This
study,
based
on
single-cell
RNA
sequencing
(scRNA-seq),
aims
to
explore
changes
endothelial
cells
(H_ECs)
osteonecrosis
femoral
head
(ONFH)
and
hip
osteoarthritis
(HOA),
focusing
death
modes
such
as
ferroptosis,
pyroptosis,
parthanatos.
We
re-analyzed
scRNA-seq
data
samples
publicly
available
2022.
study
selected
nine
(3
each
from
HOA,
ONFH
stage
3
A,
4).
CD31
+
EMCN
were
classified
H_ECs.
Molecular
differences
assessed
using
Gene
Ontology
KEGG
analysis.
Hypoxia,
parthanatos
indices
calculated,
transcription
factors
predicted
SENIC.
Cell
communication
was
analyzed
with
CellChat.
After
integrating
9
samples,
14
cell
types
identified:
B
cells,
Mesenchymal
stem
Osteoblasts,
Endothelial
Monocytes,
T
NK
Fibroblasts,
Macrophages,
Common
myeloid
progenitors,
Chondrocytes,
Myelocytes,
Osteoclasts,
Pericytes.
The
number
H_ECs
decreased
necrosis
severity.
showed
higher
angiogenic
capacity
but
lower
stress
resistance
compared
other
cells.
Angiogenic
necrotic
accompanied
by
an
elevation
inflammation
levels.
hypoxia
index
higher,
ferroptosis
increased
A
stages
4.
No
change
observed
pyroptosis.
analysis
revealed
downregulation
SLIT3-ROBO4
signaling
during
necrosis.
show
molecular
Ferroptosis
contribute
demise
ONFH,
pericytes
fibroblasts
supporting
H_EC
angiogenesis.
Language: Английский
Network pharmacology and in silico approach to study the mechanism of quercetin against breast cancer
In Silico Pharmacology,
Journal Year:
2025,
Volume and Issue:
13(1)
Published: Feb. 6, 2025
Language: Английский
Insulin-induced gene 2 alleviates ischemia-reperfusion injury in steatotic liver by inhibiting GPX4-dependent ferroptosis
Cell Death Discovery,
Journal Year:
2025,
Volume and Issue:
11(1)
Published: April 1, 2025
Abstract
Hepatic
steatosis
significantly
elevates
the
vulnerability
of
graft
to
ischemia-reperfusion
(I/R)
injury
during
liver
transplantation
(LT).
We
investigated
protective
role
insulin-induced
gene
2
(Insig2)
in
steatotic
liver’s
I/R
and
underlying
mechanisms.
Employing
mouse
model
with
Insig2
knock-out
or
hepatocyte-specific
overexpression
high-fat
diets
induce
steatosis,
we
subjected
these
mice
hepatic
injury.
The
primary
hepatocytes
isolated
from
were
used
vitro
hypoxia/reoxygenation
(H/R)
experiment.
Our
integrated
vivo
approach
uncovered
that
deficiency
exacerbated
damage
following
injury,
whereas
its
offers
protection.
Mechanically,
integrative
analysis
transcriptome,
proteome,
metabolome
found
disturbed
lipid
metabolism
oxidative
stress
homeostasis,
particularly
inhibiting
GPX4
expression
ferroptosis.
Furthermore,
chemical
inhibition
ferroptosis
reversed
deleterious
effect
deficiency;
influence
was
negated
by
target
GPX4,
leading
an
exacerbation
damage.
These
insights
underscored
potential
Insig2-GPX4
axis
as
a
therapeutic
target,
presenting
novel
avenue
for
enhancing
resilience
grafts
against
Language: Английский
The function of necroptosis in liver cancer
Mukaddas Tayir,
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Yanwen Wang,
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Ti Chu
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et al.
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease,
Journal Year:
2025,
Volume and Issue:
unknown, P. 167828 - 167828
Published: April 1, 2025
Language: Английский
The role of nutrition in cancer prevention: the effect of dietary patterns, bioactive compounds, and metabolic pathways on cancer development
Sebastián Chapela,
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Julieta Locatelli,
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Facundo Saettone
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et al.
Food and Agricultural Immunology,
Journal Year:
2025,
Volume and Issue:
36(1)
Published: April 17, 2025
Language: Английский
Caspase-independent cell death in lung cancer: from mechanisms to clinical applications
Gaurav Gupta,
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Vijaya Paul Samuel,
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M M Rekha
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et al.
Naunyn-Schmiedeberg s Archives of Pharmacology,
Journal Year:
2025,
Volume and Issue:
unknown
Published: April 21, 2025
Abstract
Caspase-independent
cell
death
(CICD)
has
recently
become
a
very
important
mechanism
in
lung
cancer,
particular,
to
overcome
critical
failure
apoptotic
that
is
common
disease
progression
and
treatment
failures.
The
pathways
involved
CICD
span
from
necroptosis,
ferroptosis,
mitochondrial
dysfunction,
autophagy-mediated
death.
Its
potential
therapeutic
applications
have
been
highlighted.
Glutathione
peroxidase
4
(GPX4)
inhibition-driven
ferroptosis
drug
resistance
non-small
cancer
(NSCLC).
In
addition,
necroptosis
involving
RIPK1
RIPK3
causes
tumor
modulation
of
immune
responses
the
microenvironment
(TME).
Mitochondrial
are
for
through
metabolic
redox
homeostasis.
Ferroptosis
amplified
by
reactive
oxygen
species
(ROS)
lipid
peroxidation
cells,
depolarization
induces
oxidative
stress
leads
mitochondria-mediated
autophagy,
or
mitophagy,
results
clearance
damaged
organelles
under
conditions,
while
this
function
also
linked
when
dysregulated.
role
autophagy
regulated
ATG
proteins
PI3K/AKT/mTOR
pathway
dual:
suppress
sensitize
cells
therapy.
A
promising
approach
enhancing
outcomes
involves
targeting
mechanisms
CICD,
including
inducing
SLC7A11
inhibition,
modulating
ROS
generation,
combining
inhibition
with
chemotherapy.
Here,
we
review
molecular
underpinnings
particularly
on
their
transform
treatment.
Language: Английский
PANoptosis: a potential target of atherosclerotic cardiovascular disease
Xiao Jin,
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Yanan Zhu,
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Lina Xing
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et al.
APOPTOSIS,
Journal Year:
2025,
Volume and Issue:
unknown
Published: April 26, 2025
PANoptosis
is
a
newly
discovered
cell
death
pathway
triggered
by
the
innate
immunizer,
which
in
turn
promotes
assembly
of
PANoptosome
and
activates
downstream
effectors.
As
special
mode,
it
characterized
apoptosis,
pyroptosis,
necroptosis
at
same
time;
therefore,
not
feasible
to
inhibit
suppressing
single
pathway.
However,
active
ingredients
targeting
can
effectively
PANoptosis.Given
importance
disease,
would
be
an
important
therapeutic
tool.
Previous
studies
have
focused
more
on
infectious
diseases
cancer,
role
cardiovascular
field
has
been
comprehensively
addressed.
While
ASCVD
number
one
killer
diseases,
explore
new
targets
determine
future
research
directions.
Therefore,
this
review
focuses
PANoptosome,
molecular
mechanism
PANoptosis,
related
mechanisms
leading
such
as
myocardial
infarction,
ischemic
cardiomyopathy
stroke,
order
provide
perspective
for
prevention
treatment
ASCVD.
Language: Английский
The Emerging Scenario of Ferroptosis in Pancreatic Cancer Tumorigenesis and Treatment
Hui Lyu,
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Jinghua Kong,
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Jiasi Chen
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et al.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(24), P. 13334 - 13334
Published: Dec. 12, 2024
Pancreatic
cancer
remains
one
of
the
most
lethal
forms
cancer.
Currently,
there
is
a
lack
effective
drug
treatments
for
pancreatic
However,
as
newly
discovered
form
non-apoptotic
cell
death,
ferroptosis
has
garnered
increasing
attention
in
relation
to
Understanding
role
tumorigenesis
and
treatment
may
enable
more
clinical
trials
minimize
side
effects
or
restrict
emergence
resistance.
In
this
review,
we
summarize
current
knowledge
regarding
process
underlying
mechanisms
ferroptosis,
well
its
dual
both
promoting
facilitating
strategies
Additionally,
how
implicated
development
pancreatitis
insulin
resistance,
indicating
that
play
an
important
risk
pancreatitis-
insulin-resistance-related
cancers,
also
addressed.
Language: Английский