Mitochondria
are
essential
organelles
responsible
for
intracellular
energy
production
and
play
crucial
roles
in
cellular
metabolism,
inflammation,
apoptosis.
Reactive
oxygen
species
(ROS)
primarily
produced
the
mitochondria
endoplasmic
reticulum
of
hepatocytes
due
to
activity
cytochrome
P450
enzymes.
Under
ideal
conditions,
cells
have
specific
molecular
mechanisms
that
manage
oxidative
stress
levels,
thus
ensuring
a
balance
between
oxidants
antioxidants.
The
interplay
ROS-induced
mitochondrial
dysfunction
activation
NLRP3
(nucleotide-binding
oligomerization
domain-like
receptor
family,
pyrin
domain
containing
3)
inflammasome
context
liver
diseases
has
been
extensively
studied.
However,
exact
by
which
promote
contribute
onset
disease
remain
unclear.
This
review
aims
elucidate
recently
discovered
regulation
disorders,
including
alcohol-related
(ALD),
metabolic-associated
steatotic
(MASLD),
hepatocellular
carcinoma
(HCC).
Finally,
it
summarizes
various
natural
pharmaceutical
agents
can
mitigate
damage
modulating
through
pathways.
work
serves
as
an
important
resource
identifying
new
therapeutic
approaches
provides
further
support
advancing
understanding
diseases.
International Journal of Molecular Sciences,
Journal Year:
2025,
Volume and Issue:
26(3), P. 1098 - 1098
Published: Jan. 27, 2025
This
article
reviews
the
synergistic
effects
of
antioxidant-enriched
functional
foods
and
exercise
in
improving
metabolic
health,
focusing
on
underlying
molecular
mechanisms.
The
review
incorporates
evidence
from
PubMed,
SCOPUS,
Web
Science,
PsycINFO,
reference
lists
relevant
up
to
20
December
2024,
highlighting
central
role
Nrf2
pathway.
As
a
critical
regulator
oxidative
stress
adaptation,
mediates
benefits
these
interventions.
presents
an
innovative
approach
understanding
regulation
inflammation,
its
potential
prevention
treatment
various
diseases,
including
cancer,
neurodegenerative
disorders,
cardiovascular
pulmonary
diabetes,
inflammatory
conditions,
ageing,
infections
such
as
COVID-19.
novelty
this
study
is
investigate
bioactive
compounds
found
(such
polyphenols,
flavonoids,
vitamins)
exercise-induced
activation
combined
reveals
their
improve
insulin
sensitivity
lipid
metabolism
reduce
offering
promising
strategy
for
management
chronic
diseases.
However,
there
are
significant
gaps
current
research,
particularly
regarding
mechanisms
interaction
between
diet,
physical
activity,
activation,
well
long-term
different
populations,
those
with
In
addition,
interactions
other
signalling
pathways,
AMPK,
NF-κB,
PI3K/Akt,
collective
contributions
health
explored.
Furthermore,
novel
biomarkers
presented
assess
impact
strategies,
NAD+/NADH
ratio,
GSH
markers
mitochondrial
health.
findings
provide
valuable
insights
into
how
integration
antioxidant-rich
diet
regular
can
by
activating
related
pathways
represent
strategies
disorders.
Further
studies
needed
fully
understand
therapeutic
interventions
diseases
stress,
disease,
cancer.
The Egyptian Journal of Internal Medicine,
Journal Year:
2024,
Volume and Issue:
36(1)
Published: Feb. 12, 2024
Abstract
Background
Liver
fibrosis
results
from
chronic
liver
injury
and
is
characterized
by
excessive
deposition
of
extracellular
matrix
proteins
including
collagen.
It
can
progress
to
cirrhosis
failure.
Main
body
the
abstract
Multiple
cellular
signaling
pathways
drive
hepatic
stellate
cell
activation
fibrogenesis.
Advances
in
biomarkers,
imaging
modalities,
omics
platforms
enable
noninvasive
diagnosis
staging
fibrosis.
Emerging
antifibrotic
approaches
include
medications
like
pirfenidone,
obeticholic
acid,
monoclonal
antibodies
targeting
pro-fibrotic
mediators.
Cell
therapies
using
mesenchymal
stem
cells
demonstrate
potential
through
paracrine
immunosuppression.
Tissue-engineered
grafts
biomaterial
carriers
for
localized
drug
delivery
are
promising
technologies.
Microfluidic
liver-on-a-chip
with
patient-derived
provide
unprecedented
models
study
human
test
candidates.
Short
conclusion
Significant
has
elucidated
mechanisms
underlying
fibrogenesis
uncovered
novel
therapeutic
targets.
Ongoing
challenges
translating
preclinical
findings,
improving
efficacy,
enabling
personalized
precision
medicine
approaches.
Further
research
into
combinatorial
therapies,
tissue
engineering
technologies
will
advance
treatment
all
causes.
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(5), P. 613 - 613
Published: May 17, 2024
Radiation
pneumonitis
(RP)
is
a
prevalent
and
fatal
complication
of
thoracic
radiotherapy
due
to
the
lack
effective
treatment
options.
RP
primarily
arises
from
mitochondrial
injury
in
lung
epithelial
cells.
The
mitochondrial-derived
peptide
MOTS-c
has
demonstrated
protective
effects
against
various
diseases
by
mitigating
injury.
C57BL/6
mice
were
exposed
20
Gy
irradiation
(IR)
received
daily
intraperitoneal
injections
for
2
weeks.
significantly
ameliorated
tissue
damage,
inflammation,
oxidative
stress
caused
radiation.
Meanwhile,
reversed
apoptosis
damage
alveolar
cells
mice.
Furthermore,
inhibited
MLE-12
primary
mouse
Mechanistically,
increased
nuclear
factor
erythroid
2-related
(Nrf2)
level
promoted
its
translocation.
Notably,
Nrf2
deficiency
abolished
function
with
RP.
In
conclusion,
alleviates
protecting
through
an
Nrf2-dependent
mechanism,
indicating
that
may
be
novel
potential
agent
Frontiers in Nutrition,
Journal Year:
2025,
Volume and Issue:
12
Published: March 4, 2025
Globally,
metabolic
dysfunction-associated
fatty
liver
disease
(MAFLD),
also
known
as
non-alcoholic
(NAFLD)
or
steatotic
(MASLD),
is
a
common
chronic
disease.
The
progression
of
MAFLD
leads
to
vicious
cycle
in
which
oxidative
stress
results
from
the
that
augmenting
de-novo
lipid
levels
and
increases
steatosis.
Most
non-enzymatic
antioxidants
are
present
food.
Therefore,
review
summarizes
findings
studies
on
food-derived
presents
an
stress-related
regulatory
network
MAFLD,
offering
new
ideas
for
prevention
treatment.
Metabolites,
Journal Year:
2025,
Volume and Issue:
15(4), P. 227 - 227
Published: March 27, 2025
Background:
The
clinical
relevance
of
circulating
cell-free
DNA
(cfDNA)
in
oncology
has
gained
significant
attention,
with
its
potential
as
a
biomarker
for
cancer
diagnosis
and
monitoring.
However,
precise
role
biology
progression
remains
unclear.
cfDNA
patients'
blood
been
shown
to
activate
signaling
pathways,
such
those
mediated
by
toll-like
receptors
(TLRs),
suggesting
involvement
cell
adaptation
the
tumor
microenvironment.
Methods:
This
impact
released
from
MDA-MB-231,
triple-negative
breast
(TNBC)
line
was
assessed,
focusing
on
glucose
availability
culture
duration.
proliferation
MDA-MB-231
cells
investigated
using
curves,
while
cellular
migration
evaluated
through
wound
healing
assays.
metabolic
alterations
induced
distinct
variants
were
nuclear
magnetic
resonance
(NMR)
spectroscopy,
their
effect
cisplatin
resistance
flow
cytometry.
Furthermore,
expression
levels
DNA-sensitive
Toll-like
receptor
9
(TLR9)
quantified
via
immunofluorescence,
alongside
colocalization
lysosome-associated
membrane
protein
1
(LAMP1).
Results:
study
indicates
that
facilitates
adaptation,
particularly
under
stress,
modulating
glutamine
consumption,
key
pathways
metabolism.
Exposure
shifts,
favoring
energy
production
oxidative
phosphorylation.
anti-cancer
activity
isolated
conditioned
media
cultured
stressful
conditions
is
influenced
duration,
emphasizing
importance
se-lection
releasing
can
drive
pro-tumoral
processes.
Additionally,
exposure
proliferation,
quiescence,
migration,
processes
linked
metastasis
treatment
resistance.
These
findings
underscore
mediator
reprogramming
adaptive
responses
cells,
contributing
therapy
activation
TLR9
suggests
mechanistic
basis
cfDNA-induced
phenotypic
changes.
Conclusions:
Overall,
serves
crucial
molecule
microenvironment,
orchestrating
enhance
survival
progression.