The Science of The Total Environment,
Journal Year:
2024,
Volume and Issue:
918, P. 170668 - 170668
Published: Feb. 5, 2024
Transient
receptor
potential
(TRP)
ankyrin
1
(TRPA1)
could
mediate
ozone-induced
lung
injury.
Optic
Atrophy
(OPA1)
is
one
of
the
significant
mitochondrial
fusion
proteins.
Impaired
fusion,
resulting
in
dysfunction
and
ferroptosis,
may
drive
onset
progression
In
this
study,
we
examined
whether
TRPA1
mediated
bronchial
epithelial
cell
injury
by
activating
PI3K/Akt
with
involvement
OPA1,
leading
to
ferroptosis.
Wild-type,
TRPA1-knockout
(KO)
mice
(C57BL/6
J
background)
ferrostatin-1
(Fer-1)-pretreated
were
exposed
2.5
ppm
ozone
for
3
h.
Human
(BEAS-2B)
cells
treated
h
presence
inhibitor
A967079
or
TRPA1-knockdown
(KD)
as
well
pharmacological
modulators
PI3K/Akt-OPA1-ferroptosis.
Transcriptome
was
used
screen
decipher
differential
gene
expressions
pathways.
Oxidative
stress,
inflammation
ferroptosis
measured
together
morphology,
function
dynamics.
Acute
exposure
induced
airway
hyperresponsiveness
(AHR),
reduced
enhanced
mice.
Similarly,
acute
inflammatory
responses,
altered
redox
abnormal
structure
function,
BEAS-2B
cells.
There
increased
decreased
responses
ozone-exposed
TRPA1-KO
Fer-1-pretreated
TRPA1-KD
OPA1
prevented
through
pathway
These
vitro
results
further
confirmed
modulator
experiments.
Exposure
induces
human
mouse
lungs
TRPA1,
which
via
a
PI3K/Akt/OPA1
axis.
This
supports
role
blockade
preventing
deleterious
effects
ozone.
APOPTOSIS,
Journal Year:
2024,
Volume and Issue:
unknown
Published: June 17, 2024
Abstract
Disulfidptosis
is
a
novel
form
of
cell
death
that
distinguishable
from
established
programmed
pathways
such
as
apoptosis,
pyroptosis,
autophagy,
ferroptosis,
and
oxeiptosis.
This
process
characterized
by
the
rapid
depletion
nicotinamide
adenine
dinucleotide
phosphate
(NADPH)
in
cells
high
expression
solute
carrier
family
7
member
11
(SLC7A11)
during
glucose
starvation,
resulting
abnormal
cystine
accumulation,
which
subsequently
induces
andabnormal
disulfide
bond
formation
actin
cytoskeleton
proteins,
culminating
network
collapse
disulfidptosis.
review
aimed
to
summarize
underlying
mechanisms,
influencing
factors,
comparisons
with
traditional
pathways,
associations
related
diseases,
application
prospects,
future
research
directions
Scientific Reports,
Journal Year:
2025,
Volume and Issue:
15(1)
Published: Jan. 2, 2025
The
impact
of
O3
on
the
respiratory
system
is
a
significant
global
problem.
Nevertheless,
there
insufficient
information
about
its
disorders
in
northeast
China.
In
this
study,
we
used
generalized
additive
model
(GAM)
to
determine
correlation
between
concentrations
and
deaths
based
daily
meteorological
data,
pollutant
concentrations,
from
2014
2016
Shenyang,
typical
city
Single
cumulative
lag
structures
seasonal
modification
were
considered
investigate
link
exposure
mortality
Synergic
effects
factors
also
evaluated.
Results
indicated
that
was
number
caused
by
diseases
basis,
regardless
time
delay
occurrence
deaths.
A
10
µg/m3
rise
concentration
associated
with
0.85%
(95%
CI
0.18–1.52%)
increase
death
at
1
day
1.43%
0.40–2.48%)
3
days.
Stratified
analyses
revealed
had
greater
health
under
warm
conditions
compared
cold
settings.
Additionally,
more
pronounced
effect
females
than
males.
results
for
study
could
provide
some
scientific
guidance
local
environment
departments.
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(2), P. 212 - 212
Published: Feb. 8, 2024
(1)
Background:
Ozone
exposure
is
a
promising
tool
for
treating
liver
damage
since
it
known
to
control
the
release
of
free
radicals
and
increase
expression
antioxidant
enzymes.
The
objective
investigate
main
intracellular
pathways
activated
after
ozone,
considering
dosage
enzymes
markers
oxidative
stress.
(2)
Methods:
This
systematic
review
was
performed
based
on
PRISMA
guidelines
using
structured
search
in
MEDLINE
(PubMed),
Scopus,
Web
Science.
Bias
analysis
methodological
quality
assessments
were
examined
SYRCLE
Risk
tool.
(3)
Results:
Nineteen
studies
selected.
results
showed
that
ozone
has
protective
effect
tissue,
promoting
decrease
inflammatory
reduction
stress
tissue.
In
addition,
also
promoted
an
morphological
consequences
controlling
these
reducing
tissue
process
areas
degeneration
necrosis.
(4)
Conclusions:
beneficial
models
injury
through
markers.
regulates
Nrf2/ARE
pathway
blocks
NF-κB
pathway.
Journal of Translational Medicine,
Journal Year:
2023,
Volume and Issue:
21(1)
Published: July 8, 2023
Osteoarthritis
(OA),
in
which
macrophage-driven
synovitis
is
considered
closely
related
to
cartilage
destruction
and
could
occur
at
any
stage,
an
inflammatory
arthritis.
However,
there
are
no
effective
targets
cure
the
progression
of
OA.
The
NOD-,
LRR-,and
pyrin
domain-containing
protein
3
(NLRP3)
inflammasome
synovial
macrophages
participates
pathological
process
treatment
strategies
targeting
it
be
approach
for
PIM-1
kinase,
as
a
downstream
effector
many
cytokine
signaling
pathways,
plays
pro-inflammatory
role
disease.In
this
study,
we
evaluated
expression
infiltration
human
OA
synovium.
effects
mechanism
were
investigated
mice
stimulated
by
lipopolysaccharide
(LPS)
different
agonists
such
nigericin,
ATP,
Monosodium
urate
(MSU),
Aluminum
salt
(Alum).
protective
on
chondrocytes
assessed
modified
co-culture
system
induced
macrophage
condition
medium
(CM).
therapeutic
effect
vivo
was
confirmed
medial
meniscus
(DMM)-induced
mice.The
increased
synovium
accompanied
macrophages.
In
vitro
experiments,
suppression
SMI-4a,
specific
inhibitor,
rapidly
inhibited
NLRP3
activation
gasdermin-D
(GSDME)-mediated
pyroptosis.
Furthermore,
inhibition
specifically
blocked
apoptosis-associated
speck-like
containing
CARD
(ASC)
oligomerization
assembly
stage.
Mechanistically,
alleviated
mitochondrial
reactive
oxygen
species
(ROS)/chloride
intracellular
channel
proteins
(CLICs)-dependent
Cl-
efflux
pathway,
eventually
resulted
blockade
ASC
activation.
showed
chondroprotective
system.
Finally,
SMI-4a
significantly
suppressed
reduced
scores
Research
Society
International
(OARSI)
score
DMM-induced
model.Therefore,
represented
new
class
promising
target
these
mechanisms
widened
road
