Ecotoxicology and Environmental Safety,
Journal Year:
2023,
Volume and Issue:
266, P. 115555 - 115555
Published: Oct. 12, 2023
Mitochondrial
dysfunction
was
reported
to
be
involved
in
the
development
of
lung
diseases
including
chronic
obstructive
pulmonary
disease
(COPD).
However,
molecular
regulation
underlying
metabolic
disorders
airway
epithelia
exposed
air
pollution
remains
unclear.
In
present
study,
bronchial
epithelial
BEAS-2B
and
alveolar
A549
cells
were
treated
with
diesel
exhaust
particles
(DEPs),
primary
representative
ambient
particle
matter.
This
treatment
elicited
cell
death
accompanied
by
induction
lipid
reactive
oxygen
species
(ROS)
production
ferroptosis.
Lipidomics
analyses
revealed
that
DEPs
increased
glycerophospholipid
contents.
Accordingly,
upregulated
expression
electron
transport
chain
(ETC)
complex
induced
mitochondrial
ROS
production.
Mechanistically,
DEP
exposure
downregulated
Hippo
transducer
transcriptional
co-activator
PDZ-binding
motif
(TAZ),
which
further
identified
crucial
for
ferroptosis-associated
antioxidant
system,
glutathione
peroxidase
4
(GPX4),
glutamate-cysteine
ligase
catalytic
subunit
(GCLC),
glutathione-disulfide
reductase
(GSR).
Moreover,
immunohistochemistry
confirmed
downregulation
GPX4
upregulation
peroxidation
epithelium
COPD
patients
Sprague-Dawley
rats
pollution.
Finally,
proteomics
alterations
ETC-related
proteins
bronchoalveolar
lavage
from
compared
healthy
subjects.
Together,
our
study
discovered
involvement
redox
dysregulation
plays
a
vital
role
destruction
after
Signal Transduction and Targeted Therapy,
Journal Year:
2023,
Volume and Issue:
8(1)
Published: Dec. 10, 2023
Abstract
Ferroptosis,
a
unique
modality
of
cell
death
with
mechanistic
and
morphological
differences
from
other
modes,
plays
pivotal
role
in
regulating
tumorigenesis
offers
new
opportunity
for
modulating
anticancer
drug
resistance.
Aberrant
epigenetic
modifications
posttranslational
(PTMs)
promote
resistance,
cancer
progression,
metastasis.
Accumulating
studies
indicate
that
can
transcriptionally
translationally
determine
vulnerability
to
ferroptosis
functions
as
driver
nervous
system
diseases
(NSDs),
cardiovascular
(CVDs),
liver
diseases,
lung
kidney
diseases.
In
this
review,
we
first
summarize
the
core
molecular
mechanisms
ferroptosis.
Then,
roles
processes,
including
histone
PTMs,
DNA
methylation,
noncoding
RNA
regulation
such
phosphorylation,
ubiquitination,
SUMOylation,
acetylation,
ADP-ribosylation,
are
concisely
discussed.
The
PTMs
genesis
cancers,
NSD,
CVDs,
well
application
PTM
modulators
therapy
these
then
discussed
detail.
Elucidating
mediated
by
will
facilitate
development
promising
combination
therapeutic
regimens
containing
or
PTM-targeting
agents
inducers
be
used
overcome
chemotherapeutic
resistance
could
prevent
addition,
highlight
potential
approaches
chemoresistance
halt
Cell Death Discovery,
Journal Year:
2025,
Volume and Issue:
11(1)
Published: Jan. 24, 2025
Abstract
Environmental
pollution
represents
a
significant
public
health
concern,
with
the
potential
risks
associated
environmental
pollutants
receiving
considerable
attention
over
an
extended
period.
In
recent
years,
substantial
body
of
research
has
been
dedicated
to
this
topic.
Since
discovery
ferroptosis,
iron-dependent
programmed
cell
death
typically
characterized
by
lipid
peroxidation,
in
2012,
there
have
advances
study
its
role
and
mechanism
various
diseases.
A
growing
number
studies
also
demonstrated
involvement
ferroptosis
damage
caused
organism
pollutants,
molecular
mechanisms
involved
partially
elucidated.
The
targeting
be
effective
means
ameliorating
PM2.5,
organic
inorganic
ionizing
radiation.
This
review
begins
providing
summary
most
important
ferroptosis.
It
then
proceeds
offer
critical
analysis
effects
induced
pollutants.
Furthermore,
as
is
case
all
rapidly
evolving
areas,
are
numerous
unanswered
questions
challenges
pertaining
pollutant-induced
which
we
discuss
attempt
provide
some
directions
clues
for
future
field.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(22), P. 16410 - 16410
Published: Nov. 16, 2023
Pulmonary
fibrosis
(PF)
is
a
chronic
interstitial
lung
disease
characterized
by
myofibroblast
abnormal
activation
and
extracellular
matrix
deposition.
However,
the
pathogenesis
of
PF
remains
unclear,
treatment
options
are
limited.
Epidemiological
studies
have
shown
that
average
age
patients
estimated
to
be
over
65
years,
incidence
increases
with
age.
Therefore,
considered
an
age-related
disease.
A
preliminary
study
on
demonstrated
combination
therapy
anti-senescence
drugs
dasatinib
quercetin
improved
physical
functional
indicators.
Given
global
aging
population
role
cellular
senescence
in
tissue
organ
aging,
understanding
impact
growing
interest.
This
article
systematically
summarizes
causes
signaling
pathways
PF.
It
also
objectively
analyzes
AECs
fibroblasts
development.
Furthermore,
potential
intervention
methods
targeting
discussed.
review
not
only
provides
strong
theoretical
foundation
for
manipulating
senescence,
developing
new
therapies
improve
diseases,
extending
healthy
lifespan
but
offers
hope
reversing
toxicity
caused
massive
accumulation
cells
humans.
Journal of Translational Internal Medicine,
Journal Year:
2024,
Volume and Issue:
12(1), P. 22 - 34
Published: Feb. 1, 2024
Abstract
Fibrosis
occurs
in
many
organs,
and
its
sustained
progress
can
lead
to
organ
destruction
malfunction.
Although
numerous
studies
on
fibrosis
have
been
carried
out,
underlying
mechanism
is
largely
unknown,
no
ideal
treatment
currently
available.
Ferroptosis
an
iron-dependent
process
of
programmed
cell
death
that
characterized
by
lipid
peroxidation.
In
the
past
decade,
a
growing
body
evidence
demonstrated
association
between
ferroptosis
fibrotic
diseases,
while
targeting
may
serve
as
potential
therapeutic
strategy.
This
review
highlights
recent
advances
crosstalk
fibrosis,
discusses
ferroptosis-targeted
approaches
against
are
being
explored.
Molecular Neurodegeneration,
Journal Year:
2024,
Volume and Issue:
19(1)
Published: April 19, 2024
Abstract
The
unprecedented
pandemic
of
COVID-19
swept
millions
lives
in
a
short
period,
yet
its
menace
continues
among
survivors
the
form
post-COVID
syndrome.
An
exponentially
growing
number
suffer
from
cognitive
impairment,
with
compelling
evidence
trajectory
accelerated
aging
and
neurodegeneration.
novel
enigmatic
nature
this
yet-to-unfold
pathology
demands
extensive
research
seeking
answers
for
both
molecular
underpinnings
potential
therapeutic
targets.
Ferroptosis,
an
iron-dependent
cell
death,
is
strongly
proposed
underlying
mechanism
post-COVID-19
neurodegeneration
discourse.
incites
neuroinflammation,
iron
dysregulation,
reactive
oxygen
species
(ROS)
accumulation,
antioxidant
system
repression,
renin-angiotensin
(RAS)
disruption,
clock
gene
alteration.
These
events
pave
way
ferroptosis,
which
shows
signature
COVID-19,
premature
aging,
neurodegenerative
disorders.
In
search
treatment,
melatonin
shines
as
promising
ferroptosis
inhibitor
repeatedly
reported
safety
tolerability.
According
to
various
studies,
has
proven
efficacy
attenuating
severity
certain
manifestations,
validating
reputation
anti-viral
compound.
Melatonin
well-documented
anti-aging
properties
combating
neurodegenerative-related
pathologies.
can
block
leading
since
it
efficient
anti-inflammatory,
chelator,
antioxidant,
angiotensin
II
antagonist,
regulator.
Therefore,
we
propose
culprit
behind
melatonin,
well-fitting
inhibitor,
treatment.
