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
Molecular Cancer,
Journal Year:
2024,
Volume and Issue:
23(1)
Published: Nov. 29, 2024
Cell
death
is
a
fundamental
part
of
life
for
metazoans.
To
maintain
the
balance
between
cell
proliferation
and
metabolism
human
bodies,
certain
number
cells
need
to
be
removed
regularly.
Hence,
mechanisms
have
been
preserved
during
evolution
multicellular
organisms.
Tumorigenesis
closely
related
with
exceptional
inhibition
death.
Mutations
or
defects
in
death-related
genes
block
elimination
abnormal
enhance
resistance
malignant
chemotherapy.
Therefore,
investigation
enables
development
drugs
that
directly
induce
tumor
In
guidelines
updated
by
Death
Nomenclature
Committee
(NCCD)
2018,
was
classified
into
12
types
according
morphological,
biochemical
functional
classification,
including
intrinsic
apoptosis,
extrinsic
mitochondrial
permeability
transition
(MPT)-driven
necrosis,
necroptosis,
ferroptosis,
pyroptosis,
PARP-1
parthanatos,
entotic
death,
NETotic
lysosome-dependent
autophagy-dependent
immunogenic
cellular
senescence
mitotic
catastrophe.
The
mechanistic
relationships
epigenetic
controls
cancer
progression
were
previously
unclear.
this
review,
we
will
summarize
pathways
corresponding
regulations.
Also,
explore
extensive
interactions
these
discuss
epigenetics
which
bring
benefits
therapy.
Frontiers in Oncology,
Journal Year:
2024,
Volume and Issue:
14
Published: March 18, 2024
In
the
last
decade,
ferroptosis
has
received
much
attention
from
scientific
research
community.
It
differs
other
modes
of
cell
death
at
morphological,
biochemical,
and
genetic
levels.
Ferroptosis
is
mainly
characterized
by
non-apoptotic
iron-dependent
caused
lipid
peroxide
excess
accompanied
abnormal
iron
metabolism
oxidative
stress.
recent
years,
more
studies
have
shown
that
closely
related
to
occurrence
development
lung
diseases.
COPD,
asthma,
injury,
fibrosis,
cancer,
infection
respiratory
diseases
become
third
most
common
chronic
worldwide,
bringing
serious
economic
psychological
burden
people
around
world.
However,
exact
mechanism
which
involved
in
progression
not
been
fully
revealed.
this
manuscript,
we
describe
ferroptosis,
targeting
signaling
pathways
proteins,
summarize
relationship
between
diseases,
explore
intervention
targeted
therapy
for
Bone Research,
Journal Year:
2024,
Volume and Issue:
12(1)
Published: Dec. 1, 2024
Abstract
Osteoporosis
(OP)
is
a
common
and
fracture-prone
skeletal
disease
characterized
by
deteriorated
trabecular
microstructure
pathologically
involving
various
forms
of
regulated
bone
cell
death.
However,
the
exact
role,
cellular
nature
regulatory
mechanisms
ferroptosis
in
OP
are
not
fully
understood.
Here,
we
reported
that
femurs
from
ovariectomized
(Ovx)
mice
exhibited
pronounced
iron
deposition,
ferroptosis,
transcriptional
suppression
key
anti-ferroptotic
factor
GPX4
(glutathione
peroxidase
4).
was
accompanied
hypermethylation
Gpx4
promoter
an
increase
DNA
methyltransferases
DNMT1/3a/3b
transcriptionally
promoted
repressive
KLF5
corepressors
NCoR
SnoN.
Conversely,
DNMT
inhibition
with
SGI-1027
reversed
hypermethylation,
ferroptotic
osteoporosis.
In
cultured
primary
cells,
ferric
ammonium
citrate
(FAC)
mimicking
loading
similarly
induced
osteoblasts
but
osteoclasts,
which
were
rescued
siRNA-mediated
individual
knockdown
1/3a/3b.
Intriguingly,
alleviated
changes
caused
FAC,
inactivator
RSL3.
More
importantly,
generated
strain
osteoblast-specific
haplo-deficient
Ob+/−
developed
spontaneous
more
severe
alterations
after
Ovx
operation,
showed
inactivation
RSL3
or
semi-knockout
largely
abolished
osteoprotective
effects
SGI-1027.
Taken
together,
our
data
suggest
epigenetic
aberration
resulting
osteoblastic
contribute
significantly
to
pathogenesis,
strategies
preserving
intervention
potentially
effective
treat
related
disorders.
medRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2025,
Volume and Issue:
unknown
Published: April 16, 2025
Abstract
Epigenetic
dysregulation,
particularly
DNA
methylation
variations,
is
implicated
in
the
pathogenesis
of
chronic
obstructive
pulmonary
disease
(COPD).
Ten-eleven
translocation
(TET)
proteins
(TET1,
TET2,
and
TET3)
regulate
gene
transcription.
Impaired
TET1
expression
was
previously
associated
with
airway
inflammation
asthma.
Here
we
investigated
TET
associations
COPD
severity.
We
found
that
reduced
peripheral
blood
mononuclear
cells
higher
sputum
neutrophil
counts,
decreased
lung
function
increased
severity
patients.
These
findings
support
a
potential
protective
role
warrant
further
mechanistic
investigations
into
actions
COPD.
