International Wound Journal,
Journal Year:
2023,
Volume and Issue:
21(2)
Published: Oct. 31, 2023
Abstract
Deep
tissue
injuries
(DTIs)
are
a
serious
type
of
pressure
that
mainly
occur
at
the
bony
prominences
and
can
develop
rapidly,
making
prevention
treatment
more
difficult.
Although
consistent
research
efforts
have
been
made
over
years,
cellular
molecular
mechanisms
contributing
to
development
DTIs
remain
unclear.
More
recently,
ferroptosis,
novel
regulatory
cell
death
(RCD)
type,
has
identified
is
morphological,
biochemical
genetic
criteria
distinct
from
apoptosis,
autophagy
other
known
pathways.
Ferroptosis
characterized
by
iron
overload,
iron‐dependent
lipid
peroxidation
shrunken
mitochondria.
We
also
note
some
pathological
features
DTI
be
key
ferroptosis
pathway.
Numerous
studies
confirmed
may
involved
in
chronic
wounds,
including
DTIs.
Here,
we
elaborate
on
basic
ferroptosis.
present
evidence
pathology
highlight
future
perspective
this
emerging
field,
desiring
provide
possibilities
for
Molecular Biomedicine,
Journal Year:
2023,
Volume and Issue:
4(1)
Published: Oct. 16, 2023
Abstract
Ferroptosis,
a
regulated
form
of
cellular
death
characterized
by
the
iron-mediated
accumulation
lipid
peroxides,
provides
novel
avenue
for
delving
into
intersection
metabolism,
oxidative
stress,
and
disease
pathology.
We
have
witnessed
mounting
fascination
with
ferroptosis,
attributed
to
its
pivotal
roles
across
diverse
physiological
pathological
conditions
including
developmental
processes,
metabolic
dynamics,
oncogenic
pathways,
neurodegenerative
cascades,
traumatic
tissue
injuries.
By
unraveling
intricate
underpinnings
molecular
machinery,
contributors,
signaling
conduits,
regulatory
networks
governing
researchers
aim
bridge
gap
between
intricacies
this
unique
mode
multifaceted
implications
health
disease.
In
light
rapidly
advancing
landscape
ferroptosis
research,
we
present
comprehensive
review
aiming
at
extensive
in
origins
progress
human
diseases.
This
concludes
careful
analysis
potential
treatment
approaches
carefully
designed
either
inhibit
or
promote
ferroptosis.
Additionally,
succinctly
summarized
therapeutic
targets
compounds
that
hold
promise
targeting
within
various
facet
underscores
burgeoning
possibilities
manipulating
as
strategy.
summary,
enriched
insights
both
investigators
practitioners,
while
fostering
an
elevated
comprehension
latent
translational
utilities.
revealing
basic
processes
investigating
possibilities,
crucial
resource
scientists
medical
aiding
deep
understanding
effects
situations.
Cell Biology and Toxicology,
Journal Year:
2024,
Volume and Issue:
40(1)
Published: March 21, 2024
Abstract
Cardiovascular
diseases
(CVDs)
are
the
main
that
endanger
human
health,
and
their
risk
factors
contribute
to
high
morbidity
a
rate
of
hospitalization.
Cell
death
is
most
important
pathophysiology
in
CVDs.
As
one
cell
mechanisms,
ferroptosis
new
form
regulated
(RCD)
broadly
participates
CVDs
(such
as
myocardial
infarction,
heart
transplantation,
atherosclerosis,
failure,
ischaemia/reperfusion
(I/R)
injury,
atrial
fibrillation,
cardiomyopathy
(radiation-induced
cardiomyopathy,
diabetes
sepsis-induced
cardiac
doxorubicin-induced
iron
overload
hypertrophic
cardiomyopathy),
pulmonary
arterial
hypertension),
involving
regulation,
metabolic
mechanism
lipid
peroxidation.
This
article
reviews
recent
research
on
regulation
its
relationship
with
occurrence
treatment
CVDs,
aiming
provide
ideas
targets
for
clinical
diagnosis
by
clarifying
latest
progress
research.
Graphical
•
The
identification,
development
history
characterization
ferroptosis.
role
different
subcellular
organelles
organelle-specific
regulators
includes
metabolism,
amino
acid
metabolism.
cardiovascular
cells
diseases.
efficacy
pathological
involved
Signal Transduction and Targeted Therapy,
Journal Year:
2025,
Volume and Issue:
10(1)
Published: Jan. 2, 2025
Abstract
Rampant
phospholipid
peroxidation
initiated
by
iron
causes
ferroptosis
unless
this
is
restrained
cellular
defences.
Ferroptosis
increasingly
implicated
in
a
host
of
diseases,
and
unlike
other
cell
death
programs
the
physiological
initiation
conceived
to
occur
not
an
endogenous
executioner,
but
withdrawal
guardians
that
otherwise
constantly
oppose
induction.
Here,
we
profile
key
ferroptotic
defence
strategies
including
regulation,
modulation
enzymes
metabolite
systems:
glutathione
reductase
(GR),
suppressor
protein
1
(FSP1),
NAD(P)H
Quinone
Dehydrogenase
(NQO1),
Dihydrofolate
(DHFR),
retinal
reductases
dehydrogenases
(RDH)
thioredoxin
(TR).
A
common
thread
uniting
all
metabolites
combat
lipid
during
dependence
on
reductant,
nicotinamide
adenine
dinucleotide
phosphate
(NADPH).
We
will
outline
how
cells
control
central
carbon
metabolism
produce
NADPH
necessary
precursors
defend
against
ferroptosis.
Subsequently
discuss
evidence
for
dysregulation
different
disease
contexts
glucose-6-phosphate
dehydrogenase
deficiency,
cancer
neurodegeneration.
Finally,
several
anti-ferroptosis
therapeutic
spanning
use
radical
trapping
agents,
dependent
redox
support
highlight
current
landscape
clinical
trials
focusing
Advanced Science,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 24, 2025
Abstract
Recipients
often
suffer
from
hyperlactatemia
during
liver
transplantation
(LT),
but
whether
exacerbates
hepatic
ischemia‐reperfusion
injury
(IRI)
after
donor
implantation
remains
unclear.
Here,
the
role
of
in
IRI
is
explored.
In
this
work,
found
to
exacerbate
ferroptosis
IRI.
Lactate‐primed
lysine
acetyltransferase
8
(KAT8)
determined
directly
lactylate
mitochondrial
phosphoenolpyruvate
carboxykinase
2
(PCK2)
at
Lys100
and
augments
PCK2
kinase
activity.
By
using
gene‐edited
mice,
evidence
indicating
that
generated.
Mechanistically,
acts
as
a
critical
inducer
by
competitively
inhibiting
Parkin‐mediated
polyubiquitination
3‐oxoacyl‐ACP
synthase
(OXSM),
thereby
leading
metabolic
remodeling
fatty
acid
synthesis
(mtFAS)
potentiation
oxidative
phosphorylation
tricarboxylic
cycle.
More
importantly,
targeting
demonstrated
markedly
ameliorate
hyperlactatemia‐mediated
Collectively,
findings
support
use
therapeutics
suppress
patients
with
LT.
Cells,
Journal Year:
2023,
Volume and Issue:
12(7), P. 1050 - 1050
Published: March 30, 2023
Ferroptosis
is
an
oxidative
damage-related,
iron-dependent
regulated
cell
death
with
intracellular
lipid
peroxide
accumulation,
which
associated
many
physiological
and
pathological
processes.
It
exhibits
unique
features
that
are
morphologically,
biochemically,
immunologically
distinct
from
other
forms.
by
iron
metabolism,
anti-oxidant
defense
systems,
as
well
various
signal
pathways.
Hypoxia,
found
in
a
group
of
conditions,
can
affect
multiple
cellular
functions
activation
the
hypoxia-inducible
factor
(HIF)
signaling
mechanisms.
Emerging
evidence
demonstrated
hypoxia
regulates
ferroptosis
certain
types
conditions.
In
this
review,
we
summarize
basic
mechanisms
regulations
hypoxia,
regulation
may
contribute
to
numerous
diseases
therapies.
Cells,
Journal Year:
2023,
Volume and Issue:
12(6), P. 867 - 867
Published: March 10, 2023
Cardiovascular
diseases
(CVDs)
are
the
principal
cause
of
disease
burden
and
death
worldwide.
Ferroptosis
is
a
new
form
regulated
cell
mainly
characterized
by
altered
iron
metabolism,
increased
polyunsaturated
fatty
acid
peroxidation
reactive
oxygen
species,
depletion
glutathione
inactivation
peroxidase
4.
Recently,
series
studies
have
indicated
that
ferroptosis
involved
in
cardiac
vascular
cells
has
key
impact
on
mechanisms
leading
to
CVDs
such
as
ischemic
heart
disease,
ischemia/reperfusion
injury,
cardiomyopathies,
failure.
In
this
article,
we
reviewed
molecular
mechanism
current
understanding
pathophysiological
role
some
cardiomyopathies.
Moreover,
comprehension
machinery
governing
cardiomyocytes
may
provide
insights
into
preventive
therapeutic
strategies
CVDs.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(17), P. 13336 - 13336
Published: Aug. 28, 2023
As
a
novel
form
of
regulated
cell
death,
ferroptosis
is
characterized
by
intracellular
iron
and
lipid
peroxide
accumulation,
which
different
from
other
death
forms
morphologically,
biochemically,
immunologically.
Ferroptosis
metabolism,
antioxidant
defense
systems
as
well
various
transcription
factors
related
signal
pathways.
Emerging
evidence
has
highlighted
that
associated
with
many
physiological
pathological
processes,
including
cancer,
neurodegeneration
diseases,
cardiovascular
ischemia/reperfusion
injury.
Noncoding
RNAs
are
group
functional
RNA
molecules
not
translated
into
proteins,
can
regulate
gene
expression
in
manners.
An
increasing
number
studies
have
shown
noncoding
RNAs,
especially
miRNAs,
lncRNAs,
circRNAs,
interfere
the
progression
modulating
ferroptosis-related
genes
or
proteins
directly
indirectly.
In
this
review,
we
summarize
basic
mechanisms
regulations
focus
on
recent
mechanism
for
types
ncRNAs
to
conditions,
will
deepen
our
understanding
regulation
provide
new
insights
employing
ferroptosis-associated
therapeutic
strategies.