Cell Death and Differentiation,
Journal Year:
2022,
Volume and Issue:
29(3), P. 467 - 480
Published: Jan. 24, 2022
Ferroptosis
is
an
iron-dependent
form
of
non-apoptotic
cell
death
characterized
by
excessive
lipid
peroxidation
and
associated
with
a
plethora
pathological
conditions
in
the
liver.
Emerging
evidence
supports
notion
that
dysregulated
metabolic
pathways
impaired
iron
homeostasis
play
role
progression
liver
disease
via
ferroptosis.
Although
molecular
mechanisms
which
ferroptosis
causes
are
poorly
understood,
several
ferroptosis-associated
genes
have
been
implicated
disease.
Here,
we
review
physiological
processing
nutrients,
our
current
understanding
metabolism,
characteristics
ferroptosis,
regulate
In
addition,
summarize
pathogenesis
disease,
including
injury,
non-alcoholic
steatohepatitis,
fibrosis,
cirrhosis,
hepatocellular
carcinoma.
Finally,
discuss
therapeutic
potential
targeting
for
managing
Advanced Materials,
Journal Year:
2019,
Volume and Issue:
31(51)
Published: Oct. 8, 2019
Abstract
Ferroptosis
is
a
newly
discovered
form
of
regulated
cell
death
that
the
nexus
between
metabolism,
redox
biology,
and
human
health.
Emerging
evidence
shows
potential
triggering
ferroptosis
for
cancer
therapy,
particularly
eradicating
aggressive
malignancies
are
resistant
to
traditional
therapies.
Recently,
there
has
been
great
deal
effort
design
develop
anticancer
drugs
based
on
induction.
Recent
advances
ferroptosis‐inducing
agents
at
intersection
chemistry,
materials
science,
biology
presented.
The
basis
summarized
first
highlight
feasibility
characteristics
therapy.
A
literature
review
inducers
(including
small
molecules
nanomaterials)
then
presented
delineate
their
design,
action
mechanisms,
applications.
Finally,
some
considerations
research
spotlighted,
followed
by
discussion
challenges
future
development
directions
this
burgeoning
field.
Frontiers in Pharmacology,
Journal Year:
2018,
Volume and Issue:
9
Published: Oct. 16, 2018
Aging
is
the
progressive
loss
of
organ
and
tissue
function
over
time.
Growing
older
positively
linked
to
cognitive
biological
degeneration
such
as
physical
frailty,
psychological
impairment,
decline.
Oxidative
stress
considered
an
imbalance
between
pro-
antioxidant
species,
which
results
in
molecular
cellular
damage.
plays
a
crucial
role
development
age-related
diseases.
Emerging
research
evidence
has
suggested
that
can
control
autoxidation
by
interrupting
propagation
free
radicals
or
inhibiting
formation
subsequently
reduce
oxidative
stress,
improve
immune
function,
increase
healthy
longevity.
Indeed,
oxidation
damage
highly
dependent
on
inherited
acquired
defects
enzymes
involved
redox-mediated
signaling
pathways.
Therefore,
molecules
with
activity
promote
aging
counteract
worth
discuss
further.
Of
particular
interest
this
article,
we
highlighted
mechanisms
antioxidants
prevention
Taken
together,
better
understanding
redox
modulation
inflammation
would
provide
useful
approach
for
potential
interventions,
promoting
Physiological Reviews,
Journal Year:
2018,
Volume and Issue:
98(2), P. 813 - 880
Published: Feb. 28, 2018
Neuronal
cell
death
occurs
extensively
during
development
and
pathology,
where
it
is
especially
important
because
of
the
limited
capacity
adult
neurons
to
proliferate
or
be
replaced.
The
concept
used
simple
as
there
were
just
two
three
types,
so
we
had
work
out
which
type
was
involved
in
our
particular
pathology
then
block
it.
However,
now
know
that
are
at
least
a
dozen
ways
for
die,
blocking
mechanism
may
not
prevent
from
dying,
non-neuronal
cells
also
contribute
neuronal
death.
We
review
here
mechanisms
by
intrinsic
extrinsic
apoptosis,
oncosis,
necroptosis,
parthanatos,
ferroptosis,
sarmoptosis,
autophagic
death,
autosis,
autolysis,
paraptosis,
pyroptosis,
phagoptosis,
mitochondrial
permeability
transition.
next
explore
development,
those
induced
axotomy,
aberrant
cell-cycle
reentry,
glutamate
(excitoxicity
oxytosis),
loss
connected
neurons,
aggregated
proteins
unfolded
protein
response,
oxidants,
inflammation,
microglia.
reassess
forms
occur
stroke
Alzheimer’s
disease,
most
pathologies
involving
discuss
why
has
been
difficult
pinpoint
involved,
if
matters,
molecular
overlap
interplay
between
subroutines,
therapeutic
implications
these
multiple
overlapping
ACS Central Science,
Journal Year:
2017,
Volume and Issue:
3(3), P. 232 - 243
Published: March 7, 2017
Ferroptosis
is
a
form
of
regulated
necrosis
associated
with
the
iron-dependent
accumulation
lipid
hydroperoxides
that
may
play
key
role
in
pathogenesis
degenerative
diseases
which
peroxidation
has
been
implicated.
High-throughput
screening
efforts
have
identified
ferrostatin-1
(Fer-1)
and
liproxstatin-1
(Lip-1)
as
potent
inhibitors
ferroptosis
−
an
activity
ascribed
to
their
ability
slow
hydroperoxides.
Herein
we
demonstrate
this
likely
derives
from
reactivity
radical-trapping
antioxidants
(RTAs)
rather
than
potency
lipoxygenases.
Although
inhibited
autoxidations
styrene
revealed
Fer-1
Lip-1
react
roughly
10-fold
more
slowly
peroxyl
radicals
reactions
α-tocopherol
(α-TOH),
they
were
significantly
reactive
α-TOH
phosphatidylcholine
bilayers
consistent
greater
relative
ferroptosis.
None
Fer-1,
Lip-1,
human
15-lipoxygenase-1
(15-LOX-1)
overexpressed
HEK-293
cells
when
assayed
at
concentrations
where
These
results
stand
stark
contrast
those
obtained
known
15-LOX-1
inhibitor
(PD146176),
was
able
inhibit
enzyme
it
effective
inhibiting
Given
likelihood
subvert
by
RTAs,
evaluated
antiferroptotic
potential
1,8-tetrahydronaphthyridinols
(hereafter
THNs):
rationally
designed
unparalleled
reactivity.
We
show
for
first
time
inherent
THNs
translates
cell
culture,
lipophilic
similarly
subverting
induced
either
pharmacological
or
genetic
inhibition
hydroperoxide-detoxifying
Gpx4
mouse
fibroblasts,
glutamate-induced
death
hippocampal
cells.
RTAs
suggest
(autoxidation)
central
process.
PROTEOMICS,
Journal Year:
2019,
Volume and Issue:
19(18)
Published: March 20, 2019
Abstract
Oxygen
is
necessary
for
aerobic
metabolism
but
can
cause
the
harmful
oxidation
of
lipids
and
other
macromolecules.
Oxidation
cholesterol
phospholipids
containing
polyunsaturated
fatty
acyl
chains
lead
to
lipid
peroxidation,
membrane
damage,
cell
death.
Lipid
hydroperoxides
are
key
intermediates
in
process
peroxidation.
The
hydroperoxidase
glutathione
peroxidase
4
(GPX4)
converts
alcohols,
this
prevents
iron
(Fe
2+
)‐dependent
formation
toxic
reactive
oxygen
species
(ROS).
Inhibition
GPX4
function
leads
peroxidation
result
induction
ferroptosis,
an
iron‐dependent,
non‐apoptotic
form
This
review
describes
species,
preventing
oxidative
link
between
dysfunction,
oxidation,
ferroptosis.
Microbial Cell Factories,
Journal Year:
2020,
Volume and Issue:
19(1)
Published: Aug. 26, 2020
Lipases
are
very
versatile
enzymes,
and
produced
the
attention
of
several
industrial
processes.
Lipase
can
be
achieved
from
sources,
animal,
vegetable,
microbiological.
The
uses
microbial
lipase
market
is
estimated
to
USD
425.0
Million
in
2018
it
projected
reach
590.2
by
2023,
growing
at
a
CAGR
6.8%
2018.
Microbial
lipases
(EC
3.1.1.3)
catalyze
hydrolysis
long
chain
triglycerides.
origins
enzymes
logically
dynamic
proficient
also
have
an
extensive
range
with
manufacturing
altered
molecules.
unique
(triacylglycerol
acyl
hydrolase)
catalyzed
hydrolysis,
esterification
alcoholysis
reactions.
Immobilization
has
made
use
accomplish
its
best
performance
hence
suitable
for
reactions
need
enhance
aroma
immobilization
Immobilized
depend
on
technique
carrier
type.
choice
concerns
usually
biocompatibility,
chemical
thermal
stability,
insolubility
under
reaction
conditions,
capability
easy
rejuvenation
reusability,
as
well
cost
proficiency.
Bacillus
spp.,
Achromobacter
Alcaligenes
Arthrobacter
Pseudomonos
bacteria
Penicillium
Fusarium
Aspergillus
fungi
screened
large
scale
production.
multipurpose
biological
catalyst
given
favorable
vision
meeting
needs
industries
such
biodiesel,
foods
drinks,
leather,
textile,
detergents,
pharmaceuticals
medicals.
This
review
represents
discussion
sources
lipases,
methods
increased
productivity
profitability
reduce
logistical
liability
environment
user.