Advances in Ferroptosis Research: A Comprehensive Review of Mechanism Exploration, Drug Development, and Disease Treatment
Pharmaceuticals,
Journal Year:
2025,
Volume and Issue:
18(3), P. 334 - 334
Published: Feb. 26, 2025
In
recent
years,
ferroptosis,
as
an
emerging
modality
of
programmed
cell
death,
has
captured
significant
attention
within
the
scientific
community.
This
comprehensive
review
meticulously
canvasses
pertinent
literature
past
few
spanning
multiple
facets.
It
delves
into
intricate
mechanisms
underpinning
tracks
evolution
its
inducers
and
inhibitors,
dissects
roles
in
a
diverse
array
diseases,
well
resultant
therapeutic
implications.
A
profound
exploration
is
conducted
functional
ferroptosis-related
molecules,
intracellular
pathways,
metabolic
cascades,
signaling
transduction
routes.
Novel
ferroptosis
inhibitors
are
introduced
detail,
covering
their
design
blueprints,
synthetic
methodologies,
bioactivity
profiles.
Moreover,
exhaustive
account
provided
regarding
involvement
malignancies,
neurodegenerative
disorders,
cardiovascular
ailments,
other
pathologies.
By
highlighting
pivotal
status
potential
regimens
various
this
aspires
to
furnish
thorough
reference
framework
for
future
investigations
clinical
translations
domain.
Language: Английский
DDR1 Targeting HOXA6 Facilitates Bladder Cancer Progression via Inhibiting Ferroptosis
Journal of Cellular and Molecular Medicine,
Journal Year:
2025,
Volume and Issue:
29(6)
Published: March 1, 2025
ABSTRACT
Ferroptosis
is
an
important
factor
affecting
the
progression
of
bladder
cancer
(BC).
Previous
studies
have
confirmed
that
discoidin
domain
receptor
1
(DDR1)
promotes
BC
progression.
However,
regulatory
mechanisms
ferroptosis
are
largely
unknown.
Therefore,
this
study
aimed
to
investigate
effects
DDR1
on
cell
ferroptosis.
Ferroptosis‐sensitive
and
‐resistant
cells
were
screened,
reverse‐transcription
quantitative
PCR
western
blotting
used
determine
expression
in
cells.
In
vitro
vivo
assays
performed
analyse
The
inducer
erastin
inhibited
TCCSUP
inhibitor
ferrostatin‐1
death
caused
by
knockdown.
increased
glutathione,
glutathione
peroxidase
4
solute
carrier
family
7
member
11
expression,
while
decreasing
malondialdehyde
Fe
2+
levels
acyl‐CoA
synthetase
long‐chain
inhibiting
epithelial
mesenchymal
transition
neurofibromin
2‐yes‐associated
protein.
These
abrogated
knockdown
homeobox
A6
(HOXA6).
targeting
HOXA6
facilitated
growth
vivo.
HOXA6.
Thus,
may
serve
as
a
potential
therapeutic
target
for
BC.
Language: Английский