Targeting ferroptosis offers therapy choice in sepsis-associated acute lung injury
European Journal of Medicinal Chemistry,
Год журнала:
2024,
Номер
283, С. 117152 - 117152
Опубликована: Дек. 8, 2024
Язык: Английский
Development of a ferroptosis-related gene prognostic model and molecular subgroups characterization in sepsis
Molecular Immunology,
Год журнала:
2025,
Номер
178, С. 1 - 11
Опубликована: Янв. 6, 2025
Язык: Английский
NAT10 induces mitochondrial dysfunction in lung epithelial cells by acetylating HMGB1 to exacerbate Pseudomonas aeruginosa-induced acute lung injury
Microbial Pathogenesis,
Год журнала:
2025,
Номер
unknown, С. 107364 - 107364
Опубликована: Фев. 1, 2025
Язык: Английский
Theabrownins improve burn-induced kidney injury by increasing the levels of guanidinoacetic acid and fumaric acid
Phytomedicine,
Год журнала:
2025,
Номер
140, С. 156609 - 156609
Опубликована: Март 7, 2025
Язык: Английский
NAT10 Regulates LPS-Induced Inflammation via Stabilization of N4-Acetylated PTX3 mRNA in Human Dental Pulp Stem Cells
International Journal of Molecular Sciences,
Год журнала:
2025,
Номер
26(9), С. 4325 - 4325
Опубликована: Май 2, 2025
Severe
dental
pulp
inflammation
can
lead
to
tissue
lysis
and
destruction,
underscoring
the
necessity
for
effective
treatment
of
pulpitis.
N-acetyltransferase
10
(NAT10)-mediated
N4-acetylcytidine
(ac4C)
modification
has
recently
emerged
as
a
key
regulator
in
inflammatory
processes.
However,
whether
NAT10
affects
response
human
stem
cells
(hDPSCs)
remains
unelucidated.
In
this
study,
elevated
expression
was
observed
pulpitis
tissues
LPS-stimulated
hDPSCs.
Knockdown
led
reduced
gene
lower
reactive
oxygen
species
(ROS)
production
hDPSCs,
while
chemotactic
migration
macrophages
also
suppressed.
Similar
results
were
when
hDPSCs
treated
with
Remodelin,
an
inhibitor
NAT10.
Differentially
expressed
genes
identified
through
RNA
sequencing
significantly
enriched
signaling
pathways
after
depletion.
Among
differential
genes,
pentraxins
3
(PTX3)
potential
target
due
presence
ac4C
site
its
known
ability
regulate
inflammation.
The
mRNA
protein
levels
PTX3
NAT10-deficient
cells,
along
decrease
stability.
Exogenous
supplementation
partially
reversed
inhibition
induced
by
knockdown.
Further
evidence
vivo
revealed
that
Remodelin
attenuated
severity
rats
summary,
these
data
indicated
deficiency
inhibited
stability
further
hDPSC
inflammation,
might
be
therapeutic
agent
capping.
Язык: Английский
PARP3 promotes macrophage inflammation via mono ADP ribosylation of Ppia Glu140
Molecular Medicine,
Год журнала:
2025,
Номер
31(1)
Опубликована: Июнь 3, 2025
Acute
lung
injury
(ALI)
carries
significant
mortality
with
limited
targeted
therapies.
Macrophages
drive
early
inflammatory
propagation
in
ALI,
exacerbating
pulmonary
inflammation.
While
ADP-ribosylation
is
a
dynamic
and
reversible
post-translational
modification
(PTM)
associated
diseases,
its
role
macrophage-mediated
inflammation
remains
unclear.
Murine
ALI
model
was
established
via
intratracheal
instillation
lipopolysaccharide
(LPS).
The
tissues
cultured
mouse
macrophage
line
(RAW264.7)
treated
LPS
were
used
to
assess
the
expression
of
poly
ADP-ribose
polymerases
(Parps).
RNA
sequencing
(RNA-seq)
identified
differentially
expressed
genes
(DEGs)
following
Parp3
knockdown
(siParp3)
LPS-stimulated
RAW264.7
cells,
subsequent
pathway
analysis
transcription
factors
(TFs)
profiling
gene
ontology
(GO)
enrichment.
In
peptidyl-prolyl
cis-trans
isomerase
A
(Ppia)
modulated
by
siRNA
or
plasmid
transfection.
PARP3-Ppia
interaction
assessed
immunoprecipitation.
Modification
alterations
due
mutations
at
Ppia
sites
Enzyme-linked
immune
sorbent
assay
(ELISA)
quantify
secretion.
evaluate
lung-protective
therapeutic
effects
PARP3
inhibitor
ME0328
detecting
cytokines,
phosphorylation
p65
histopathology.
induced
cells
tissues,
correlating
elevated
cytokines.
52
overlapping
DEGs
mainly
enriched
Toll-like
receptor
(TLR)
signaling
pathway.
promoted
NF-κB
activation.
blocked
activation
tissues.
Immunoprecipitation
confirmed
that
interacted
Ppia.
modified
mono
ADP-ribosylation.
Ppia-E140
most
related
site.
mutation
E140
inhibited
response,
secretion
vivo,
reduced
alleviated
edema
mitigated
histopathological
damage.
We
as
downstream
mediated
for
promote
through
Our
findings
provide
evidence
on
Understanding
regulation
from
may
insight
into
pro-inflammatory
mechanisms
opportunities
effective
treat
acute
injury.
Язык: Английский