Clinical and Experimental Otorhinolaryngology,
Journal Year:
2023,
Volume and Issue:
17(1), P. 64 - 77
Published: Dec. 28, 2023
Objectives.
Hypoxia-inducible
factor
1α
(HIF1α)
and
Tet
methylcytosine
dioxygenase
2
(TET2)
have
been
reported
to
mediate
nasal
polypogenesis
through
the
epithelial-to-mesenchymal
transition
(EMT).
Additionally,
HIF1α
can
regulate
expression
function
of
TET2.
However,
precise
mechanism
how
TET2
regulates
EMT
mediation
in
epithelial
cells
is
still
poorly
understood.Methods.
Nasal
tissue
samples
were
collected
from
patients
with
chronic
rhinosinusitis
(CRS)
polyps
(CRSwNP),
CRS
without
(CRSsNP),
controls.
The
was
detected
using
Western
blotting
immunohistochemistry.
markers
(E-cadherin
vimentin)
also
evaluated
by
Primary
human
(hNECs)
stimulated
CoCl2
mimic
hypoxia.
Vitamin
C
(VC),
a
non-specific
activator,
small
interfering
RNA
(siRNA)
transfection
used
further
determine
role
hypoxia-induced
EMT.
Finally,
reactive
oxygen
species
(ROS)
Nrf2
measured
explore
downstream
consequences
hypoxic
hNECs.Results.
levels
lower
epithelium
CRSwNP
positively
correlated
E-cadherin
but
negatively
vimentin
CRS.
exhibited
opposite
pattern
expression.
CoCl2-simulated
hypoxia
led
increased
hNECs
vitro,
simultaneous
downregulation
Addition
VC
activated
hNECs,
inhibited
Furthermore,
siRNA
knockdown
contributed
despite
addition
VC.
regulated
ROS
generation.Conclusion.
<i>in
vivo</i>.
downregulated
HIF1α,
resulting
CoCl2-hypoxic
via
regulation
oxidative
stress
vitro</i>.
Hence,
might
provide
new
therapeutic
approach
for
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(24), P. 13617 - 13617
Published: Dec. 19, 2024
People,
in
increasing
numbers,
are
seeking
orthodontic
treatment
to
correct
malocclusion,
while
some
of
them
suffering
from
orthodontically
induced
inflammatory
root
resorption
(OIIRR).
Recent
evidence
suggests
that
the
immune-inflammatory
response
occurring
during
bone
remodeling
may
be
responsible
for
OIIRR.
Ferroptosis,
a
new
type
programmed
cell
death
(PCD),
has
been
found
have
close
interrelation
with
inflammation
disease
progression.
While
ferroptosis
extensively
studied
bone-related
diseases,
its
role
OIIRR
is
poorly
understood.
Considering
tooth
shares
lot
similar
characteristics
bone,
it
reasonable
hypothesize
contributes
development
Nevertheless,
direct
supporting
this
theory
currently
lacking.
In
review,
we
introduced
and
elucidated
mechanisms
underlying
movement
(OTM)
OIIRR,
special
focus
on
pivotal
plays
these
processes.
Additionally,
covered
recent
research
exploring
connections
between
ferroptosis.
Lastly,
emphasized
important
regulatory
function
homeostasis.
Further
investigations
required
clarify
modulation
develop
novel
potential
therapeutic
strategies
management
Allergologia et Immunopathologia,
Journal Year:
2024,
Volume and Issue:
52(4), P. 60 - 67
Published: July 1, 2024
Background:
Chronic
obstructive
pulmonary
disease
(COPD)
is
a
familiar
disease,
and
owns
high
morbidity
mortality,
which
critically
damages
the
health
of
patients.
Ubiquitin-specific
peptidase
8
(USP8)
pivotal
protein
to
join
in
regulation
some
diseases.
In
previous
report,
it
was
determined
that
USP8
expression
down-regulated
LPS-treated
BEAS-2B
cells,
restrains
inflammatory
response
accelerates
cell
viability.
However,
regulatory
roles
on
ferroptosis
COPD
are
rarely
reported,
associated
molecular
mechanisms
keep
vague.
Objective:
To
investigate
functions
progression.
Material
Methods:
The
lung
were
measured
through
Buxco
Fine
Pointe
Series
Whole
Body
Plethysmography
(WBP).
Fe
level
tested
assay
kit.
expressions
assessed
western
blot.
levels
tumor
necrosis
-factor-α,
interleukin
6,
evaluated
enzyme-linked
immunosorbent
serologic
assay.
Cell
viability
CCK-8
Results:
this
work,
discovered
overexpression
improved
function
mice.
addition,
repressed
by
regulating
glutathione
peroxidase
4
acyl-CoA
synthetase
long-chain
family
Overexpression
suppressed
inflammation
Furthermore,
model.
At
last,
verified
accelerated
ubiquitin
aldehyde-binding
1
(OTUB1)/solute
carrier
7
member
11
(SLC7A11)
pathway.
Conclusion:
This
study
manifested
restrained
OTUB1/SLC7A11
signaling
discovery
hinted
could
be
potential
target
for
treatment.
Research Square (Research Square),
Journal Year:
2024,
Volume and Issue:
unknown
Published: May 7, 2024
Abstract
Osteoporosis
(OP)
is
a
common
and
fracture-prone
skeletal
disease
featured
by
deteriorated
trabecular
microstructure
pathologically
involves
various
forms
of
regulated
bone
cell
death.
However,
the
role
regulatory
mechanisms
ferroptosis
in
OP
are
not
fully
understood.
Our
study
showed
marked
iron
deposition,
ferroptosis,
core
anti-ferroptotic
factor
GPX4
(glutathione
peroxidase
4)
suppression
femurs
ovariectomized
(Ovx)
mice,
coinciding
with
Gpx4
promoter
hypermethylation
elevated
DNMT1/3a/3b
levels.
In
addition,
KLF5,
along
transcriptional
corepressors
NCoR
SnoN,
induces
binding
to
hypermethylated
osteoporotic
sensitive
DNMT
inhibition.
Conversely,
inhibition
SGI-1027
reversed
suppression,
reducing
ferroptotic
damage.
cultured
primary
cells,
ferric
ammonium
citrate
(FAC)
mimicking
loading
similarly
induced
osteoblasts,
but
osteoclasts,
which
were
rescued
siRNA-mediated
individual
knockdown
1/3a/3b
respectively.
Intriguingly,
relieved
alterations
FAC,
inactivator
RSL3.
More
importantly,
we
generated
strain
osteoblast-specific
haplo-deficient
mice
(Gpx4+/-)
that
developed
spontaneous
further
demonstrated
inactivation
RSL3
or
osteoblastic
haplo-deficiency
largely
abrogated
osteoprotective
effects
SGI-1027.
Together,
our
data
suggest
aberration-incurred
epigenetic
resultant
contribute
significantly
pathogenesis
strategies
preserving
intervention
potentially
effective
treat
related
disorders.
International Journal of COPD,
Journal Year:
2024,
Volume and Issue:
Volume 19, P. 2073 - 2095
Published: Sept. 1, 2024
To
employ
bioinformatics
and
machine
learning
to
predict
the
characteristics
of
immune
cells
genes
associated
with
inflammatory
response
ferroptosis
in
chronic
obstructive
pulmonary
disease
(COPD)
patients
aid
development
targeted
traditional
Chinese
medicine
(TCM).
Mendelian
randomization
analysis
elucidates
causal
relationships
among
cells,
genes,
COPD,
offering
novel
insights
for
early
diagnosis,
prevention,
treatment
COPD.
This
approach
also
provides
a
fresh
perspective
on
use
treating
Clinical and Experimental Otorhinolaryngology,
Journal Year:
2023,
Volume and Issue:
17(1), P. 64 - 77
Published: Dec. 28, 2023
Objectives.
Hypoxia-inducible
factor
1α
(HIF1α)
and
Tet
methylcytosine
dioxygenase
2
(TET2)
have
been
reported
to
mediate
nasal
polypogenesis
through
the
epithelial-to-mesenchymal
transition
(EMT).
Additionally,
HIF1α
can
regulate
expression
function
of
TET2.
However,
precise
mechanism
how
TET2
regulates
EMT
mediation
in
epithelial
cells
is
still
poorly
understood.Methods.
Nasal
tissue
samples
were
collected
from
patients
with
chronic
rhinosinusitis
(CRS)
polyps
(CRSwNP),
CRS
without
(CRSsNP),
controls.
The
was
detected
using
Western
blotting
immunohistochemistry.
markers
(E-cadherin
vimentin)
also
evaluated
by
Primary
human
(hNECs)
stimulated
CoCl2
mimic
hypoxia.
Vitamin
C
(VC),
a
non-specific
activator,
small
interfering
RNA
(siRNA)
transfection
used
further
determine
role
hypoxia-induced
EMT.
Finally,
reactive
oxygen
species
(ROS)
Nrf2
measured
explore
downstream
consequences
hypoxic
hNECs.Results.
levels
lower
epithelium
CRSwNP
positively
correlated
E-cadherin
but
negatively
vimentin
CRS.
exhibited
opposite
pattern
expression.
CoCl2-simulated
hypoxia
led
increased
hNECs
vitro,
simultaneous
downregulation
Addition
VC
activated
hNECs,
inhibited
Furthermore,
siRNA
knockdown
contributed
despite
addition
VC.
regulated
ROS
generation.Conclusion.
<i>in
vivo</i>.
downregulated
HIF1α,
resulting
CoCl2-hypoxic
via
regulation
oxidative
stress
vitro</i>.
Hence,
might
provide
new
therapeutic
approach
for
