International Journal of Medical Toxicology and Forensic Medicine,
Journal Year:
2024,
Volume and Issue:
13(04), P. 43485 - 43485
Published: Jan. 28, 2024
Background:
Ferroptosis,
an
oxidative
and
iron-dependent
cell
death,
is
a
new
type
of
regulated
death.
There
are
few
studies
on
the
mechanisms
ferroptosis
in
skin
related
diseases.
Arsenic
shown
to
induce
This
study
aimed
decipher
relationship
between
arsenic
exposure
death
skin.
Methods:
Arsenic-gene
interactions
were
obtained.
Then,
skin-specific
arsenic-gene
screened.
Ferroptosis-related
genes
identified.
Analysis
functional
biological
was
performed
identify
possible
mechanisms.
Results:
The
ferroptosis-related
showed
overlap
59
genes.
Functional
enrichment,
protein-protein
interaction,
transcription
factor
(TF)/miRNA
target
gene
interaction
analyses
used
look
into
mechanism
arsenic-induced
ACTB,
CTNNB1,
HSPA8,
SRC,
RACK1,
CD44,
SQSTM1
identified
as
key
proteins.
Gene
ontology
analysis
these
proteins
indicated
mitochondrial
morphology
functionality
changes
following
HIF1A
SP1
TFs
regulate
large
number
compared
other
TFs.
Ten
miRNAs
with
high
ferroptosis-associated
Conclusion:
work
investigated
regulators,
highlighted
role
mitochondria
this
exposure.
Cell Death Discovery,
Journal Year:
2024,
Volume and Issue:
10(1)
Published: Jan. 24, 2024
Abstract
Ferroptosis
represents
a
distinct
form
of
programmed
cell
death
triggered
by
excessive
iron
accumulation
and
lipid
peroxidation-induced
damage.
This
mode
differentiates
from
classical
in
terms
morphology
biochemistry.
stands
out
for
its
exceptional
biological
characteristics
has
garnered
extensive
research
conversations
as
death.
Its
dysfunctional
activation
is
closely
linked
to
the
onset
diseases,
particularly
inflammation
cancer,
making
ferroptosis
promising
avenue
combating
these
conditions.
As
such,
exploring
may
offer
innovative
approaches
treating
cancer
inflammatory
diseases.
Our
review
provides
insights
into
relevant
regulatory
mechanisms
ferroptosis,
examining
impact
ferroptosis-related
factors
both
physiological
pathological
perspectives.
Describing
crosstalk
between
tumor-
inflammation-associated
signaling
pathways
potential
inducers
overcoming
drug-resistant
cancers
are
discussed,
aiming
inform
further
novel
therapeutic
directions
relation
Redox Biology,
Journal Year:
2024,
Volume and Issue:
71, P. 103119 - 103119
Published: March 11, 2024
Alzheimer's
disease
(AD)
is
a
neurodegenerative
disorder
characterized
by
the
build-up
of
extracellular
amyloid
β
(Aβ)
plaques
and
intracellular
neurofibrillary
tangles
(NFTs).
Ferroptosis,
an
iron
(Fe)-dependent
form
cell
death
plays
significant
role
in
multifaceted
AD
pathogenesis
through
generation
reactive
oxygen
species
(ROS),
mitochondrial
damage,
lipid
peroxidation,
reduction
glutathione
peroxidase
4
(GPX4)
enzyme
activity
levels.
Aberrant
liquid-liquid
phase
separation
(LLPS)
tau
drives
growth
maturation
NFTs
contributing
to
pathogenesis.
In
this
study,
we
strategically
combined
structural
functional
properties
gallic
acid
(GA)
cyclic
dipeptides
(CDPs)
synthesize
hybrid
molecules
that
effectively
target
both
ferroptosis
toxicity
AD.
This
innovative
approach
marks
paradigm
shift
from
conventional
therapeutic
strategies.
first
report
synthetic
small
molecule
(GCTR)
combats
ferroptosis,
simultaneously
restoring
enzymatic
enhancing
cellular
levels
its
master
regulator,
GPX4.
Further,
GCTR
disrupts
Fe3+-induced
LLPS
tau,
aids
attenuation
abnormal
fibrillization.
The
synergistic
action
combating
toxicity,
bolstered
GPX4
enhancement
modulation
LLPS,
holds
promise
for
development
molecule-based
novel
therapeutics
Cellular and Molecular Life Sciences,
Journal Year:
2023,
Volume and Issue:
80(9)
Published: Aug. 19, 2023
Abstract
Iron-dependent
lipid
peroxidation
causes
ferroptosis,
a
form
of
regulated
cell
death.
Crucial
steps
in
the
formation
ferroptosis
include
accumulation
ferrous
ions
(Fe
2+
)
and
peroxidation,
which
are
controlled
by
glutathione
peroxidase
4
(GPX4).
Its
crucial
role
stopping
spread
cancer
has
been
shown
numerous
studies
undertaken
last
ten
years.
Epithelial–mesenchymal
transition
(EMT)
is
process
epithelial
cells
acquire
mesenchymal
characteristics.
EMT
connected
to
carcinogenesis,
invasiveness,
metastasis,
therapeutic
resistance
cancer.
It
range
internal
external
signals
changes
phenotype
from
like.
Studies
have
that
tend
be
more
ferroptotic
than
their
counterparts.
Drug-resistant
easily
killed
inducers
when
they
undergo
EMT.
Therefore,
understanding
interaction
between
will
help
identify
novel
treatment
targets.
In-depth
discussion
given
regulation
potential
application
cancer,
relationships
EMT,
signaling
pathways
associated
with
tumors.
Invasion,
inflammation
all
The
goal
this
review
provide
suggestions
for
future
research
practical
guidance
applying
clinical
practice.
Frontiers in Immunology,
Journal Year:
2023,
Volume and Issue:
14
Published: Nov. 15, 2023
Psoriasis
is
a
systemic
inflammatory
disease
that
frequently
coexists
with
various
other
conditions,
such
as
essential
hypertension,
diabetes,
metabolic
syndrome,
and
bowel
disease.
The
association
between
these
diseases
may
be
attributed
to
shared
pathways
abnormal
immunomodulatory
mechanisms.
Furthermore,
metabolites
also
play
regulatory
role
in
the
function
of
different
immune
cells
involved
psoriasis
pathogenesis,
particularly
T
lymphocytes.
In
this
review,
we
have
summarized
current
research
progress
on
cell
metabolism
psoriasis,
encompassing
regulation
glucose
metabolism,
lipid
amino
acid
within
affected
by
psoriasis.
We
will
explore
interaction
mechanism
psoriatic
cells.
Moreover,
further
discussed
metabolomics
gain
deeper
understanding
its
pathogenesis
identify
potential
new
therapeutic
targets
through
identification
biomarkers
associated
condition.
Animal Models and Experimental Medicine,
Journal Year:
2023,
Volume and Issue:
6(6), P. 508 - 517
Published: Dec. 1, 2023
Abstract
Circular
RNA
(circRNA),
classified
as
a
type
of
non‐coding
RNA,
has
gained
significant
attention
in
the
field
biology
due
to
its
distinctive
ring
structure
and
functional
properties.
Recent
research
provided
evidence
that
specific
circRNAs
have
ability
modulate
disease
progression
through
diverse
mechanisms,
one
which
is
by
regulating
cellular
ferroptosis.
Ferroptosis
form
regulated
cell
death
driven
iron
dependency
lipid
peroxidation,
extensive
investigations
revealed
relationship
between
ferroptosis
development.
In
addition
both
exert
critical
roles
progression,
also
been
shown
actively
mediate
process
The
therefore
influences
offers
novel
targets
for
treatment.
By
directly
or
indirectly
modulating
expression
regulate
ferroptosis‐related
proteins,
it
may
be
possible
impact
promoting
inhibiting
Current
indicates
such
approaches
hold
value
wide
variety
common
diseases
across
physiological
systems.
This
review
comprehensively
summarizes
findings
recent
studies
investigating
regulation
various
diseases.
