Antioxidants,
Journal Year:
2025,
Volume and Issue:
14(3), P. 264 - 264
Published: Feb. 25, 2025
Autophagy
is
a
fundamental
cellular
process
that
maintains
homeostasis
by
degrading
damaged
components
and
regulating
stress
responses.
It
plays
crucial
role
in
cancer
biology,
including
tumor
progression,
metastasis,
therapeutic
resistance.
Oxidative
stress,
similarly,
key
to
maintaining
balance
oxidants
antioxidants,
with
its
disruption
leading
molecular
damage.
The
interplay
between
autophagy
oxidative
particularly
significant,
as
reactive
oxygen
species
(ROS)
act
both
inducers
by-products
of
autophagy.
While
can
function
suppressor
early
stages,
it
often
shifts
pro-tumorigenic
advanced
disease,
aiding
cell
survival
under
adverse
conditions
such
hypoxia
nutrient
deprivation.
This
dual
mediated
several
signaling
pathways,
PI3K/AKT/mTOR,
AMPK,
HIF-1α,
which
coordinate
the
autophagic
activity
ROS
production.
In
this
review,
we
explore
mechanisms
interact
across
different
hematological
malignancies.
We
discuss
how
triggers
autophagy,
creating
feedback
loop
promotes
survival,
dysregulation
leads
increased
accumulation,
exacerbating
tumorigenesis.
also
examine
implications
targeting
autophagy-oxidative
axis
cancer.
Current
strategies
involve
modulating
through
specific
inhibitors,
enhancing
levels
pro-oxidant
compounds,
combining
these
approaches
conventional
therapies
overcome
drug
Understanding
complex
relationship
provides
critical
insights
into
novel
aimed
at
improving
treatment
outcomes.
iScience,
Journal Year:
2024,
Volume and Issue:
27(3), P. 109221 - 109221
Published: Feb. 15, 2024
Fat
infiltration
in
skeletal
muscle
(also
known
as
myosteatosis)
is
now
recognized
a
distinct
disease
from
sarcopenia
and
directly
related
to
declining
capacity.
Hence,
understanding
the
origins
regulatory
mechanisms
of
fat
vital
for
maintaining
development
improving
human
health.
In
this
article,
we
summarized
triggering
factors
such
aging,
metabolic
diseases
syndromes,
nonmetabolic
diseases,
injury
that
all
induce
muscle.
We
discussed
recent
advances
on
cellular
found
several
cell
types
including
myogenic
cells
non-myogenic
contribute
myosteatosis.
Furthermore,
reviewed
molecular
mechanism,
detection
methods,
intervention
strategies
Based
current
findings,
our
review
will
provide
new
insight
into
regulating
function
lipid
metabolism
treating
muscle-related
diseases.
FEBS Letters,
Journal Year:
2024,
Volume and Issue:
598(10), P. 1301 - 1327
Published: Feb. 7, 2024
A
hallmark
of
cancer
cells
is
their
remarkable
ability
to
efficiently
adapt
favorable
and
hostile
environments.
Due
a
unique
metabolic
flexibility,
tumor
can
grow
even
in
the
absence
extracellular
nutrients
or
stressful
scenarios.
To
achieve
this,
need
large
amounts
lipids
build
membranes,
synthesize
lipid‐derived
molecules,
generate
energy
other
nutrients.
Tumor
potentiate
strategies
obtain
from
cells,
pathways
new
lipids,
mechanisms
for
efficient
storage,
mobilization,
utilization
these
lipids.
Lipid
droplets
(LDs)
are
organelles
that
collect
supply
eukaryotes
it
increasingly
recognized
accumulation
LDs
cells.
Furthermore,
an
active
role
LD
proteins
processes
underlying
tumorigenesis
has
been
proposed.
Here,
by
focusing
on
three
major
classes
LD‐resident
(perilipins,
lipases,
acyl‐CoA
synthetases),
we
provide
overview
contribution
progression
discuss
during
proliferation,
invasion,
metastasis,
apoptosis,
stemness
International Journal of Molecular Sciences,
Journal Year:
2025,
Volume and Issue:
26(2), P. 788 - 788
Published: Jan. 18, 2025
Diets
rich
in
carbohydrate
and
saturated
fat
contents,
when
combined
with
a
sedentary
lifestyle,
contribute
to
the
development
of
obesity
metabolic
syndrome
(MetS),
which
subsequently
increase
palmitic
acid
(PA)
levels.
At
high
concentrations,
PA
induces
lipotoxicity
through
several
mechanisms
involving
endoplasmic
reticulum
(ER)
stress,
mitochondrial
dysfunction,
inflammation
cell
death.
Nevertheless,
there
are
endogenous
strategies
mitigate
PA-induced
its
unsaturation
elongation
channeling
storage
lipid
droplets
(LDs),
plays
crucial
role
sequestering
oxidized
lipids,
thereby
reducing
oxidative
damage
membranes.
While
extended
exposure
promotes
reactive
oxygen
species
(ROS)
generation
leading
damage,
acute
ß-cells
increases
glucose-stimulated
insulin
secretion
(GSIS),
activation
free
fatty
receptors
(FFARs).
Subsequently,
FFARs
by
exogenous
agonists
has
been
suggested
as
potential
therapeutic
strategy
prevent
ß
cells.
Moreover,
some
acids,
including
oleic
acid,
can
counteract
negative
impact
on
cellular
health,
suggesting
complex
interaction
between
different
dietary
fats
outcomes.
Therefore,
challenge
is
peroxidation
unsaturated
acids
utilization
natural
antioxidants.
This
complexity
indicates
necessity
for
further
research
into
function
diverse
pathological
conditions
find
main
target
against
lipotoxicity.
The
aim
this
review
is,
therefore,
examine
recent
data
regarding
mechanism
underlying
order
identify
that
promote
protection
lipotoxicity,
dysfunction
apoptosis
MetS
obesity.
Molecular Neurodegeneration,
Journal Year:
2025,
Volume and Issue:
20(1)
Published: Jan. 27, 2025
Alzheimer's
disease
(AD)
is
among
the
most
devastating
neurodegenerative
disorders
with
limited
treatment
options.
Emerging
evidence
points
to
involvement
of
lipid
dysregulation
in
development
AD.
Nevertheless,
precise
lipidomic
landscape
and
mechanistic
roles
lipids
pathology
remain
poorly
understood.
This
review
aims
highlight
significance
lipidomics
lipid-targeting
approaches
diagnosis
We
summarized
connection
between
human
brain
AD
at
both
genetic
species
levels.
briefly
introduced
technologies
discussed
potential
challenges
areas
future
advancements
field
for
research.
To
elucidate
central
role
converging
multiple
pathological
aspects
AD,
we
reviewed
current
knowledge
on
interplay
major
features,
including
amyloid
beta,
tau,
neuroinflammation.
Finally,
assessed
progresses
obstacles
lipid-based
therapeutics
proposed
strategies
leveraging
Antioxidants,
Journal Year:
2025,
Volume and Issue:
14(2), P. 201 - 201
Published: Feb. 10, 2025
Oxidative
stress
is
a
common
event
involved
in
cancer
pathophysiology,
frequently
accompanied
by
unique
lipid
metabolic
reprogramming
phenomena.
caused
mainly
an
imbalance
between
the
production
of
reactive
oxygen
species
(ROS)
and
antioxidant
system
cells.
Emerging
evidence
has
reported
that
oxidative
regulates
expression
activity
metabolism-related
enzymes,
leading
to
alteration
cellular
metabolism;
this
involves
significant
increase
fatty
acid
synthesis
shift
way
which
lipids
are
taken
up
utilized.
The
dysregulation
metabolism
provides
abundant
intermediates
synthesize
biological
macromolecules
for
rapid
proliferation
cells;
moreover,
it
contributes
maintenance
intracellular
redox
homeostasis
producing
variety
reducing
agents.
Moreover,
derivatives
metabolites
play
critical
roles
signal
transduction
within
cells
tumor
microenvironment
evades
immune
destruction
facilitates
invasion
metastasis.
These
findings
suggest
close
relationship
during
malignant
progression
cancers.
This
review
focuses
on
crosstalk
reprogramming,
in-depth
insight
into
modulation
ROS
cancers
discusses
potential
strategies
targeting
therapy.