Antioxidants,
Год журнала:
2025,
Номер
14(3), С. 265 - 265
Опубликована: Фев. 25, 2025
Bee
pollen
(BP)
is
one
of
the
richest
known
natural
resources
micronutrients
and
bioactive
phytochemicals.
Some
captivating
bioactivities
BP
compounds,
although
being
largely
investigated
for
latter
as
individual
molecules,
remain
very
scarcely
or
completely
uninvestigated
in
bee
a
whole
product.
Among
most
intriguing
these
bioactivities,
we
identified
ferroptosis
major
one.
Ferroptosis,
recently
discovered
form
cell
death
(connecting
oxidative
stress
inflammation),
complex
pathophysiological
process
crucial
perplexing
events
current
challenging
human
diseases
such
cancer,
neurodegeneration,
general
aging
diseases.
Many
compounds
were
found
to
intricately
modulate
depending
on
cellular
context
by
inducing
this
mechanism
malignant
cells
preventing
it
non-malignant
cells.
Since
research
both
fields,
i.e.,
ferroptosis,
still
recent,
deemed
necessary
undertake
review
figure
out
extent
potential
modulating
mechanisms.
Our
proved
that
wide
range
(polyphenols,
phenolamides,
carotenoids,
vitamins,
minerals,
others)
substantially
diverse
Accordingly,
phytochemicals
nutrients
showed
interesting
preclinical
studies
lead
ferroptosis-mediated
outcomes
important
processes,
including
many
aging-related
disorders.
One
paramount
challenges
be
resolved
determine
how
different
act
biological
contexts,
either
through
synergistic
antagonistic
behaviors.
We
hope
our
work
constitutes
valuable
incentive
future
investigations
promising
relevant
avenue.
Medicine,
Год журнала:
2024,
Номер
103(9), С. e37360 - e37360
Опубликована: Март 1, 2024
Oxidative
stress,
a
condition
characterized
by
an
imbalance
between
reactive
oxygen
species
(ROS)
production
and
the
body's
ability
to
detoxify
them,
has
emerged
as
pivotal
factor
in
pathophysiology
of
various
diseases.
Red
blood
cells
(RBCs),
essential
components
circulatory
system,
are
particularly
susceptible
oxidative
damage
due
their
high
oxygen-carrying
capacity
abundance
vulnerable
biomolecules.
This
review
comprehensively
explores
intricate
mechanisms
underlying
stress-induced
red
subsequent
implications
for
overall
health
disease.
We
delve
into
sources
ROS
generation
within
RBCs,
including
metabolic
processes
external
factors,
shedding
light
on
delicate
redox
balance
that
governs
cellular
homeostasis.
The
impact
stress
extends
beyond
confines
primary
physiological
role,
these
actively
participate
immune
responses,
inflammation
modulation,
nitric
oxide
metabolism.
Consequently,
understanding
RBCs
provides
valuable
insights
broader
landscape
In
conclusion,
this
underscores
critical
role
influencing
cell
physiology
its
far-reaching
human
health.
Elucidating
molecular
intricacies
relationship
not
only
enhances
our
fundamental
biological
but
also
paves
way
development
targeted
therapeutic
interventions
mitigate
adverse
effects
and,
extension,
Antioxidants,
Год журнала:
2024,
Номер
13(3), С. 298 - 298
Опубликована: Фев. 28, 2024
Ferroptosis
is
a
type
of
programmed
cell
death
that
differs
from
apoptosis,
autophagy,
and
necrosis
related
to
several
physio-pathological
processes,
including
tumorigenesis,
neurodegeneration,
senescence,
blood
diseases,
kidney
disorders,
ischemia–reperfusion
injuries.
linked
iron
accumulation,
eliciting
dysfunction
antioxidant
systems,
which
favor
the
production
lipid
peroxides,
membrane
damage,
ultimately,
death.
Thus,
signaling
pathways
evoking
ferroptosis
are
strongly
associated
with
those
protecting
cells
against
excess
and/or
lipid-derived
ROS.
Here,
we
discuss
interaction
between
metabolic
particular
focus
on
transcription
factors
implicated
in
regulation
ferroptosis,
either
as
triggers
peroxidation
or
defense
pathways.
Signal Transduction and Targeted Therapy,
Год журнала:
2025,
Номер
10(1)
Опубликована: Янв. 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
Cell Death and Disease,
Год журнала:
2024,
Номер
15(7)
Опубликована: Июль 4, 2024
Abstract
Autoimmune
diseases
commonly
affect
various
systems,
but
their
etiology
and
pathogenesis
remain
unclear.
Currently,
increasing
research
has
highlighted
the
role
of
ferroptosis
in
immune
regulation,
with
cells
being
a
crucial
component
body’s
system.
This
review
provides
an
overview
discusses
relationship
between
ferroptosis,
programmed
cell
death
cells,
autoimmune
diseases.
Additionally,
it
summarizes
key
targets
such
as
GPX4
TFR,
responses.
Furthermore,
release
multiple
molecules,
including
damage-associated
molecular
patterns
(DAMPs),
following
by
is
examined,
these
molecules
further
influence
differentiation
function
thereby
affecting
occurrence
progression
Moreover,
secrete
factors
or
metabolites,
which
also
impact
target
organs
tissues
involved
Iron
chelators,
chloroquine
its
derivatives,
antioxidants,
calreticulin
have
been
demonstrated
to
be
effective
animal
studies
for
certain
diseases,
exerting
anti-inflammatory
immunomodulatory
effects.
Finally,
brief
summary
future
perspectives
on
are
provided,
aiming
guide
disease
treatment
strategies.
Cell
death
is
one
of
the
most
important
mechanisms
maintaining
homeostasis
in
our
body.
Ferroptosis
and
pyroptosis
are
forms
necrosis-like
cell
death.
These
modalities
play
key
roles
pathophysiology
cancer,
cardiovascular,
neurological
diseases,
other
pathologies.
Transition
metals
abundant
group
elements
all
living
organisms.
This
paper
presents
a
summary
ferroptosis
pathways
their
connection
to
significant
transition
metals,
namely
zinc
(Zn),
copper
(Cu),
molybdenum
(Mo),
lead
(Pb),
cobalt
(Co),
iron
(Fe),
cadmium
(Cd),
nickel
(Ni),
mercury
(Hg),
uranium
(U),
platinum
(Pt),
crucial
element,
selenium
(Se).
Authors
aim
summarize
up-to-date
knowledge
this
topic.In
review,
there
categorized
highlighted
common
patterns
alterations
by
metals.
Special
attention
given
since
collected
data
support
its
dual
nature
action
both
pyroptosis.
All
findings
presented
together
with
brief
description
major
biochemical
involving
mentioned
visualized
attached
comprehensive
figures.This
work
concludes
that
majority
disruptions
studied
metals'
impacts
fate,
influencing
survival
cells
complex
system
altered
pathways.
Therefore,
opens
up
space
for
further
research.
Ferroptosis
is
a
recently
discovered
form
of
regulated
cell
death
characterized
by
its
distinct
dependence
on
iron
and
the
peroxidation
lipids
within
cellular
membranes.
plays
crucial
role
in
physiological
pathological
situations
has
attracted
attention
numerous
scientists.
suppressive
protein
1
(FSP1)
one
main
regulators
that
negatively
regulates
ferroptosis
through
GPX4-independent
FSP1-CoQ10-NAD(P)H
axis
potential
therapeutic
target
for
ferroptosis-related
diseases.
However,
crystal
structure
FSP1
not
been
resolved,
which
hinders
development
strategies
targeting
FSP1.
To
unravel
this
puzzle,
we
purified
human
(hFSP1)
using
baculovirus
eukaryotic
expression
system
solved
at
resolution
1.75
Å.
Furthermore,
evaluated
oxidoreductase
activity
hFSP1
with
NADH
as
substrate
identified
E156
key
amino
acid
maintaining
activity.
Interestingly,
our
results
indicated
exists
functions
monomeric
state.
Mutagenesis
analysis
revealed
critical
C-terminal
domain
binding
substrate.
These
findings
significantly
enhance
understanding
functional
mechanism
provide
precise
model
further
drug
development.