Deciphering the Power of Resveratrol in Mitophagy: From Molecular Mechanisms to Therapeutic Applications
Phytotherapy Research,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 4, 2025
Resveratrol
(RES),
a
natural
polyphenolic
compound,
has
garnered
significant
attention
for
its
therapeutic
potential
in
various
pathological
conditions.
This
review
explores
how
RES
modulates
mitophagy-the
selective
autophagic
degradation
of
mitochondria
essential
maintaining
cellular
homeostasis.
promotes
the
initiation
and
execution
mitophagy
by
enhancing
PINK1/Parkin-mediated
mitochondrial
clearance,
reducing
reactive
oxygen
species
production,
mitigating
apoptosis,
thereby
preserving
integrity.
Additionally,
regulates
through
activation
key
molecular
targets
such
as
AMP-activated
protein
kinase
(AMPK),
mechanistic
target
rapamycin
(mTOR),
deacetylases
(SIRT1
SIRT3),
quality
control
(MQC)
pathways,
demonstrating
substantial
effects
multiple
disease
models.
We
provide
detailed
account
biosynthetic
pharmacokinetics,
metabolic
characteristics
RES,
focusing
on
role
modulation
implications
medical
applications.
Potential
adverse
associated
with
clinical
use
are
also
discussed.
Despite
promising
properties,
application
is
limited
issues
bioavailability
pharmacokinetic
profiles.
Future
research
should
concentrate
developing
derivatives
that
precisely
modulate
mitophagy,
unlocking
new
avenues
therapy.
Language: Английский
Predicting Which Mitophagy Proteins Are Dysregulated in Spinocerebellar Ataxia Type 3 (SCA3) Using the Auto-p2docking Pipeline
International Journal of Molecular Sciences,
Journal Year:
2025,
Volume and Issue:
26(3), P. 1325 - 1325
Published: Feb. 4, 2025
Dysfunctional
mitochondria
are
present
in
many
neurodegenerative
diseases,
such
as
spinocerebellar
ataxia
type
3
(SCA3),
also
known
Machado–Joseph
disease
(MJD).
SCA3/MJD,
the
most
frequent
worldwide,
is
caused
by
abnormal
expansion
of
polyglutamine
tract
(polyQ)
at
ataxin-3.
This
protein
to
deubiquitinate
key
proteins
Parkin,
which
required
for
mitophagy.
Ataxin-3
interacts
with
Beclin1
(essential
initiating
autophagosome
formation
adjacent
mitochondria),
well
mitochondrial
cristae
TBK1.
To
identify
other
mitophagy
pathway
(according
KEGG
database)
that
can
interact
ataxin-3,
here
we
developed
a
pipeline
silico
analyses
protein–protein
interactions
(PPIs),
called
auto-p2docking.
Containerized
Docker,
auto-p2docking
ensures
reproducibility
and
reduces
number
errors
through
its
simplified
configuration.
Its
architecture
consists
22
modules,
used
develop
12
protocols
but
be
specified
according
user
needs.
In
this
work,
45
putative
ataxin-3
interactors
(53%
novel),
using
interacting
regions
validation.
Furthermore,
predict
from
both
Parkin-independent
-dependent
mechanisms
affected
polyQ
expansion.
Language: Английский
Galectin-8 drives ERK-dependent mitochondrial fragmentation, perinuclear relocation and mitophagy, with metabolic adaptations for cell proliferation
European Journal of Cell Biology,
Journal Year:
2025,
Volume and Issue:
unknown, P. 151488 - 151488
Published: April 1, 2025
Mitochondria
adapt
to
the
cell
proliferative
demands
induced
by
growth
factors
through
dynamic
changes
in
morphology,
distribution,
and
metabolic
activity.
Galectin-8
(Gal-8),
a
carbohydrate-binding
protein
that
promotes
proliferation
transactivating
EGFR-ERK
signaling
pathway,
is
overexpressed
several
cancers.
However,
its
impact
on
mitochondrial
dynamics
during
remains
unknown.
Using
MDCK
RPTEC
kidney
epithelial
cells,
we
demonstrate
Gal-8
induces
fragmentation
perinuclear
redistribution.
Additionally,
mitochondria
adopt
donut-shaped
morphologies,
live-cell
imaging
with
two
Keima-based
reporters
demonstrates
Gal-8-induced
mitophagy.
ERK
inhibition
abrogates
all
these
proliferation.
Studies
established
mutant
versions
of
CHO
cells
reveal
response
require
interactions
between
N-terminal
carbohydrate
recognition
domain
α-2,3-sialylated
N-glycans
at
surface.
DRP1,
key
regulator
fission,
becomes
phosphorylated
or
an
ERK-dependent
manner,
mediating
Bafilomycin
A
proliferation,
suggesting
mitophagy
serves
as
adaptation
demands.
Functional
analysis
under
stimulation
shows
maintain
active
electron
transport
chain,
partially
uncoupled
from
ATP
synthesis,
increased
membrane
potential,
indicative
healthy
mitochondria.
Meanwhile,
exhibit
extracellular
acidification
rate
lactate
production
via
aerobic
glycolysis,
hallmark
state.
Our
findings
integrate
adaptations
potential
implications
for
physiology,
disease,
therapeutic
strategies.
Language: Английский
From Childhood Obesity to Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) and Hyperlipidemia Through Oxidative Stress During Childhood
Siham Accacha,
No information about this author
Julia Barillas-Cerritos,
No information about this author
Ankita Srivastava
No information about this author
et al.
Metabolites,
Journal Year:
2025,
Volume and Issue:
15(5), P. 287 - 287
Published: April 24, 2025
Background/Objectives:
Metabolic
dysfunction-associated
steatotic
liver
disease
(MASLD),
previously
known
as
non-alcoholic
fatty
(NAFLD),
is
rapidly
becoming
the
most
prevalent
form
of
chronic
in
both
pediatric
and
adult
populations.
It
encompasses
a
wide
spectrum
abnormalities,
ranging
from
simple
fat
accumulation
to
severe
conditions
such
inflammation,
fibrosis,
cirrhosis,
cancer.
Major
risk
factors
for
MASLD
include
obesity,
insulin
resistance,
type
2
diabetes,
hypertriglyceridemia.
Methods:
This
narrative
review
employed
comprehensive
search
recent
literature
identify
latest
studies
on
relationship
between
MAFLD
health
consequences
treatment
options
prevent
long-term
damage
other
organs.
Additionally,
article
presents
perspectives
diagnostic
biomarkers.
Results:
Childhood
obesity
linked
multitude
comorbid
remains
primary
factor
obesity.
abnormal
have
detrimental
effects
into
adulthood.
Scientific
evidence
unequivocally
demonstrates
role
obesity-related
conditions,
dyslipidemia,
hyperglycemia,
development
progression
MASLD.
Oxidative
stress,
stemming
mitochondrial
dysfunction,
leading
discusses
interconnections
oxidative
Conclusions:
Atherogenic
endothelial
cytokines
collectively
contribute
Potential
targets
are
focused
prevention
use
drugs
address
elevated
blood
lipid
levels.
Language: Английский
Mitochondrial proteins as therapeutic targets in diabetic ketoacidosis: evidence from Mendelian randomization analysis
Ruiqiang Xie,
No information about this author
Hongyan Xie,
No information about this author
Hong Gao
No information about this author
et al.
Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
15
Published: Oct. 14, 2024
Introduction
Diabetic
ketoacidosis
(DKA)
is
a
severe
and
potentially
fatal
acute
complication
in
diabetic
patients,
commonly
occurring
type
1
diabetes
(T1D)
but
also
seen
2
(T2D).
The
pathogenesis
of
DKA
involves
complex
physiological
processes
that
are
not
fully
understood,
especially
the
role
mitochondria.
Mitochondria,
known
as
powerhouse
cells,
plays
crucial
oxidative
phosphorylation
ATP
production,
which
vital
various
metabolic
diseases,
including
diabetes.
However,
exact
causal
relationship
between
mitochondrial
dysfunction
remains
unclear.
Methods
This
study
employed
Mendelian
randomization
(MR)
analysis
protein-protein
interaction
(PPI)
networks
to
systematically
explore
relationships
DNA
copy
number
(mtDNA-CN)
specific
proteins
with
DKA.
We
used
bidirectional
MR
genome-wide
association
(GWAS)
data
from
openGWAS
database
investigate
effects
mtDNA-CN
64
mitochondrial-related
on
its
subtypes
(T1DKA,
T2DKA,
unspecified-DKA).
Results
revealed
increased
significantly
reduces
risk
DKA,
whereas
effect
was
significant.
Mitochondrial-related
such
MRPL32,
MRPL33,
COX5B,
DNAJC19,
NDUFB8
showed
negative
indicating
their
potential
protective
roles.
Conversely,
ATP5F1B
COX4I2
have
positive
excessive
production
patients
may
be
detrimental
health
increase
complications
Discussion
results
emphasize
necessity
protecting
function
order
reduce
offers
novel
perspectives
molecular
pathways
involved
emphasizing
critical
functions
mt-DNA
distinct
proteins.
These
evidences
only
enhance
our
comprehension
implications
diabetes-related
identify
therapeutic
targets
for
individualized
treatment
approaches,
thereby
making
substantial
contribution
clinical
care
public
initiatives.
Language: Английский
The Role of Endothelial Cell Mitophagy in Age-Related Cardiovascular Diseases
Quancheng Han,
No information about this author
Yiding Yu,
No information about this author
Xiujuan Liu
No information about this author
et al.
Aging and Disease,
Journal Year:
2024,
Volume and Issue:
unknown, P. 0 - 0
Published: Jan. 1, 2024
Aging
is
a
major
risk
factor
for
cardiovascular
diseases
(CVD),
and
mitochondrial
autophagy
impairment
considered
significant
physiological
change
associated
with
aging.
Endothelial
cells
play
crucial
role
in
maintaining
vascular
homeostasis
function,
participating
various
processes
such
as
regulating
tone,
coagulation,
angiogenesis,
inflammatory
responses.
As
aging
progresses,
endothelial
worsens,
leading
to
the
development
of
numerous
diseases.
Therefore,
vital
preventing
treating
age-related
However,
there
currently
lack
systematic
reviews
this
area.
To
address
gap,
we
have
written
review
provide
new
research
therapeutic
strategies
managing
Language: Английский
Mitophagy Unveiled: Exploring the Nexus of Mitochondrial Health and Neuroendocrinopathy
Journal of Molecular Neuroscience,
Journal Year:
2024,
Volume and Issue:
74(4)
Published: Nov. 8, 2024
Language: Английский
Insights into the role of mitophagy in lung cancer: current evidence and perspectives
Xin Zhang,
No information about this author
Dongzhi Yu,
No information about this author
Peng Tang
No information about this author
et al.
Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
15
Published: June 19, 2024
Lung
cancer,
recognized
globally
as
a
leading
cause
of
malignancy-associated
morbidity
and
mortality,
is
marked
by
its
high
prevalence
lethality,
garnering
extensive
attention
within
the
medical
community.
Mitophagy
critical
cellular
process
that
plays
crucial
role
in
regulating
metabolism
ensuring
quality
control
cells.
Its
relevance
to
lung
cancer
has
garnered
significant
among
researchers
scientists.
Mitophagy’s
involvement
encompasses
initiation,
progression,
metastatic
dissemination
treatment.
The
regulatory
landscape
mitophagy
complex,
involving
numerous
signaling
proteins
pathways
may
exhibit
aberrant
alterations
or
mutations
tumor
environment.
In
field
treatment,
regulation
considered
key
determining
chemotherapy,
radiation
therapy,
other
treatment
options,
drug
resistance.
Contemporary
investigations
are
directed
towards
harnessing
modulators,
both
inhibitors
activators,
therapeutic
strategies,
with
an
emphasis
on
achieving
specificity
minimize
collateral
damage
healthy
populations.
Furthermore,
molecular
constituents
affiliated
mitophagy,
serving
potential
biomarkers,
offer
promising
avenues
for
enhancing
diagnostic
accuracy,
prognostic
assessment,
prediction
responses
cancer.
Future
endeavors
will
also
involve
investigating
impact
composition
function
immune
cells
microenvironment,
aiming
enhance
our
understanding
how
modulates
response
This
review
aims
comprehensively
overview
recent
advancements
about
genesis,
progenesis
metastasis,
We
discussed
future
research
direction
Language: Английский
The phytochemical composition and unexplored potential of Australian native plants for application in physical activity-related muscle recovery and inflammation: a literature review
Food & Function,
Journal Year:
2024,
Volume and Issue:
15(19), P. 9718 - 9733
Published: Jan. 1, 2024
Native
plants
are
adaptable
in
various
environmental
conditions
part
through
the
production
of
unique
phytochemicals
which
may
have
beneficial
effects
on
human
health.
Language: Английский