Ferroptosis and hearing loss: from molecular mechanisms to therapeutic interventions
Xiaozhen Lv,
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Chenyi Yang,
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Xianying Li
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et al.
Journal of Enzyme Inhibition and Medicinal Chemistry,
Journal Year:
2025,
Volume and Issue:
40(1)
Published: Feb. 24, 2025
Hearing
loss
profoundly
affects
social
engagement,
mental
health,
cognition,
and
brain
development,
with
sensorineural
hearing
(SNHL)
being
a
major
concern.
Linked
to
ototoxic
medications,
ageing,
noise
exposure,
SNHL
presents
significant
treatment
challenges,
highlighting
the
need
for
effective
prevention
regeneration
strategies.
Ferroptosis,
distinct
form
of
cell
death
featuring
iron-dependent
lipid
peroxidation,
has
garnered
interest
due
its
potential
role
in
cancer,
neuronal
degeneration,
especially
loss.
The
emerging
ferroptosis
as
crucial
mediator
suggests
that
it
may
offer
novel
therapeutic
target
otoprotection.
This
review
aims
summarise
intricate
connection
between
SNHL,
offering
fresh
perspective
exploring
targeted
strategies
could
potentially
mitigate
cochlear
cells
damage
enhance
quality
life
individuals
impairments.
Language: Английский
The role of ferroptosis in neurodegenerative diseases
Yifan Fei,
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Yunjie Ding
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Frontiers in Cellular Neuroscience,
Journal Year:
2024,
Volume and Issue:
18
Published: Oct. 15, 2024
Ferroptosis
represents
an
iron
−
and
lipid
peroxidation
(LPO)-mediated
form
of
regulated
cell
death
(RCD).
Recent
evidence
strongly
suggests
the
involvement
ferroptosis
in
various
neurodegenerative
diseases
(NDs),
particularly
Alzheimer’s
disease
(AD),
Parkinson’s
(PD),
Huntington’s
(HD),
multiple
sclerosis
(MS),
amyotrophic
lateral
(ALS),
among
others.
The
treatment
poses
both
opportunities
challenges
context
ND.
This
review
provides
a
comprehensive
overview
characteristic
features,
induction
inhibition
ferroptosis,
highlighting
inhibitor
underlying
mechanisms
responsible
for
its
occurrence.
Moreover,
explores
how
these
contribute
to
pathogenesis
progression
major
disorders.
Additionally,
it
presents
novel
insights
into
role
ND
summarizes
recent
advancements
development
therapeutic
approaches
targeting
ferroptosis.
These
hold
potential
guide
future
strategies
aimed
at
effectively
managing
debilitating
medical
conditions.
Language: Английский
Ferroptosis in the neurovascular unit after spinal cord injury
Yushan Huang,
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Jinzhu Bai
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Experimental Neurology,
Journal Year:
2024,
Volume and Issue:
381, P. 114943 - 114943
Published: Sept. 4, 2024
Language: Английский
Natural products protect against spinal cord injury by inhibiting ferroptosis: a literature review
Wei She,
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Jian‐Qiang Su,
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Wenjian Ma
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et al.
Frontiers in Pharmacology,
Journal Year:
2025,
Volume and Issue:
16
Published: April 3, 2025
Spinal
cord
injury
(SCI)
is
a
severe
traumatic
condition
that
frequently
results
in
various
neurological
disabilities,
including
significant
sensory,
motor,
and
autonomic
dysfunctions.
Ferroptosis,
recently
identified
non-apoptotic
form
of
cell
death,
characterized
by
the
accumulation
reactive
oxygen
species
(ROS),
intracellular
iron
overload,
lipid
peroxidation,
ultimately
culminating
death.
Recent
studies
have
demonstrated
ferroptosis
plays
critical
role
pathophysiology
SCI,
contributing
significantly
to
neural
demise.
Three
key
cellular
enzymatic
antioxidants
such
as
glutathione
peroxidase
4
(GPX4),
suppressor
protein
1
(FSP1),
dihydroorotate
dehydrogenase
(DHODH),
been
elucidated
crucial
components
defense
against
ferroptosis.
Natural
products,
which
are
bioactive
compounds
mostly
derived
from
plants,
garnered
considerable
attention
for
their
potential
therapeutic
effects.
Numerous
reported
several
natural
products
can
effectively
mitigate
death
alleviate
SCI
symptoms.
This
review
summarizes
fifteen
containing
(-)-Epigallocatechin-3-gallate
(EGCG),
Proanthocyanidin,
Carnosic
acid,
Astragaloside
IV,
Trehalose,
8-gingerol,
Quercetin,
Resveratrol,
Albiflorin,
Alpha-tocopherol,
Celastrol,
Hispolon,
Dendrobium
Nobile
Polysaccharide,
Silibinin,
Tetramethylpyrazine
shown
promise
treating
inhibiting
Additionally,
this
provides
an
overview
mechanisms
involved
these
proposes
perspectives
guide
future
research
directions.
Language: Английский
Analyzing the role of ferroptosis in ribosome‐related bone marrow failure disorders: From pathophysiology to potential pharmacological exploitation
IUBMB Life,
Journal Year:
2024,
Volume and Issue:
76(12), P. 1011 - 1034
Published: July 25, 2024
Abstract
Within
the
last
decade,
scientific
community
has
witnessed
importance
of
ferroptosis
as
a
novel
cascade
molecular
events
leading
to
cellular
decisions
death
distinct
from
apoptosis
and
other
known
forms
cell
death.
Notably,
such
non‐
apoptotic
iron‐dependent
regulated
been
found
be
intricately
linked
several
physiological
processes
well
pathogenesis
various
diseases.
To
this
end,
recent
data
support
notion
that
potential
connection
between
inherited
bone
marrow
failure
(IBMF)
in
individuals
with
ribosomopathies
may
exist.
In
review,
we
suggest
ribosome‐related
IBMFs
identified
mutations
ribosomal
proteins
lead
changes
ribosome
composition
hematopoietic
progenitors,
seem
affect
function,
thus
enhancing
expression
some
mRNAs
subgroups
while
reducing
others.
These
an
imbalance
inside
pathways
are
promoted
others
inhibited.
This
disturbance
is
accompanied
by
ROS
production
lipid
peroxidation,
additional
finding
most
them
iron
accumulation.
Once
peroxidation
accumulation
two
main
characteristics
ferroptosis,
it
possible
mechanism
plays
key
role
manifestation
IBMF
type
disease.
If
further
confirmed,
new
pharmacological
targets
inhibitors
already
exploited
for
treatment
diseases,
could
utilized
improve
ribosomopathies.
Language: Английский
Physiologic Regulation of Lipid Oxidation and Ferroptosis By Vitamin E, High-Density Lipoprotein, and Scavenger Receptor Class B Type 1
Jonathan S. Rink,
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Andrea E. Calvert,
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Alexandra Moxley
No information about this author
et al.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: Nov. 15, 2024
ABSTRACT
Ferroptosis
is
a
form
of
cell
death
caused
by
oxidative
(-OOH)
damage
to
phospholipids
(PL)
that
comprise
the
membrane.
Understanding
mechanisms
ferroptosis
important
because
role
it
plays
in
human
disease,
including
cancer
and
neurodegeneration.
Previous
work
has
focused
on
intracellular
antioxidant
enzyme
glutathione
peroxidase
4
(GPx4),
which
detoxifies
PL-peroxides
(PL-OOH)
prevents
ferroptosis.
Studies
also
show
alpha-tocopherol
(α-toc),
active
Vitamin
E,
an
exogenous
lipophilic
inhibits
cells
vitro
neurons
hematopoietic
stem
vivo.
The
α-toc
engages
manipulate
PL
redox
balance
are
unknown.
Lipoproteins,
like
high-
low-density
lipoproteins
(HDL
LDL),
carry
circulation,
compelled
our
investigation
their
delivery
Using
neuronal
models,
here
we
lipoproteins,
particularly
HDL,
deliver
binding
membrane
receptor
scavenger
class
B
type
1
(SR-B1)
prevent
Additionally,
synthesized
SR-B1
targeted
HDL-like
particles
contained
validate
data
obtained
with
native
lipoproteins.
We
reveal
tunable
cellular
axis
whereby
synthetic
HDLs
containing
target
reduce
PL-OOH
Language: Английский
Mechanisms of Vitamins Inhibiting Ferroptosis
Meng Zhang,
No information about this author
Xin Chen,
No information about this author
Yumei Zhang
No information about this author
et al.
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(12), P. 1571 - 1571
Published: Dec. 20, 2024
Ferroptosis
is
an
iron-dependent
form
of
cell
death,
which
characterized
by
the
uncontrolled
and
overwhelming
peroxidation
membrane
lipids.
has
been
implicated
in
progression
various
pathologies,
including
steatotic
liver,
heart
failure,
neurodegenerative
diseases,
diabetes.
Targeted
inhibition
ferroptosis
provides
a
promising
strategy
to
treat
ferroptosis-related
diseases.
Multivitamins,
vitamins
A,
B,
C,
D,
E,
K,
have
shown
good
ability
inhibit
ferroptosis.
For
example,
vitamin
A
significantly
upregulated
expression
several
key
ferroptotic
gatekeepers
genes
through
nuclear
retinoic
acid
receptors
X
(RAR/RXR).
Vitamin
B6
could
compensate
for
impaired
glutathione
(GSH)
levels
restore
Glutathione
peroxidase
4
(GPX4)
cells,
ultimately
inhibiting
D
up-regulate
anti-ferroptosis
proteins
activating
receptors.
E
hydroquinone
K
(VKH2)
can
directly
propagation
lipid
peroxidation,
thereby
In
this
review,
we
summarize
currently
understood
mechanisms
provide
reference
information
future
research
on
development
inhibitors.
Language: Английский