Cells,
Journal Year:
2024,
Volume and Issue:
13(24), P. 2115 - 2115
Published: Dec. 20, 2024
The
mammalian
Apolipoprotein-L
families
(APOLs)
contain
several
isoforms
of
membrane-interacting
proteins,
some
which
are
involved
in
the
control
membrane
dynamics
(traffic,
fission
and
fusion).
Specifically,
human
APOL1
APOL3
appear
to
remodeling
linked
pathogen
infection.
Through
its
association
with
Non-Muscular
Myosin-2A
(NM2A),
controls
Golgi-derived
trafficking
vesicles
carrying
lipid
scramblase
Autophagy-9A
(ATG9A).
These
deliver
together
phosphatidylinositol-4-kinase-B
(PI4KB)
activated
Stimulator
Interferon
Genes
(STING)
mitochondrion-endoplasmic
reticulum
(ER)
contact
sites
(MERCSs)
for
induction
completion
mitophagy
apoptosis.
direct
interactions
PI4KB
activity
controllers
(Neuronal
Calcium
Sensor-1,
or
NCS1,
Calneuron-1,
CALN1,
ADP-Ribosylation
Factor-1,
ARF1),
PI(4)P
synthesis.
is
required
different
processes
infection-induced
inflammation:
(i)
STING
activation
at
Golgi
subsequent
lysosomal
degradation
inflammation
termination;
(ii)
mitochondrion
MERCSs
apoptosis;
(iii)
phagolysosome
formation
antigen
processing.
In
addition,
governs
mitophagosome
fusion
endolysosomes
completion,
APOL3-like
murine
APOL7C
phagosome
permeabilization
cross-presentation
dendritic
cells.
Similarly,
can
induce
intracellular
bacterial
membranes,
a
role
also
be
proposed
endothelial
APOLd1
adipocyte
mAPOL6,
promote
angiogenesis
adipogenesis,
respectively,
under
inflammatory
conditions.
Thus,
APOL
play
distinct
roles
associated
inflammation.
Frontiers in Immunology,
Journal Year:
2025,
Volume and Issue:
15
Published: Jan. 6, 2025
Hepatocellular
carcinoma
(HCC)
is
a
common
malignant
tumor
of
the
digestive
system
with
high
incidence
that
seriously
threatens
patients'
lives
and
health.
However,
rise
application
new
treatments,
such
as
immunotherapy,
there
are
still
some
restrictions
in
treatment
diagnosis
HCC,
therapeutic
effects
on
patients
not
ideal.
Two
single-cell
RNA
sequencing
(scRNA-seq)
datasets
from
HCC
patients,
encompassing
25,189
cells,
were
analyzed
study.
We
utilized
non-negative
matrix
factorization
(NMF)
clustering
to
identify
mitophagy
patterns
TME
including
cancer-associated
fibroblasts
(CAFs),
T
B
tumor-associated
macrophages
(TAMs).
Cell-to-cell
communication
was
using
CellChat
package,
pseudotime
trajectory
analysis
performed
Monocle
package.
Gene
regulatory
networks
investigated
SCENIC
survival
analyses
conducted
mitophagy-related
signatures.
samples
identified
22
clusters,
7
principal
cell
types.
Complex
communications
observed
among
these
Mitophagy-related
CAFs,
TAMs,
CD8+
cells
identified.
These
subtypes
had
different
biological
states,
cell-cell
communications,
metabolic
pathways.
Mitophagy
levels
elevated
samples.
Changes
genes
within
specific
associated
overall
rates.
did
seem
affect
effectiveness
immunotherapy.
This
study
provides
evidence
modulates
intercellular
communication,
influencing
progression
patient
prognosis.
Targeting
may
offer
promising
approach
improve
long-term
prognosis
patients.
Cornea,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 17, 2025
Purpose:
To
investigate
the
effectiveness
of
mitochondrial-targeted
antioxidant
mitoquinone
(MitoQ)
and
nontargeted
idebenone
(Idb)
in
alleviating
mitochondrial
dysfunction
corneal
endothelial
cells
(CEnCs).
Methods:
In
vitro
experiments
were
conducted
using
immortalized
normal
human
(HCEnC-21T;
SVN1-67F)
Fuchs
dystrophy
(FECD)
(SVF5-54F;
SVF3-76M).
Cells
pretreated
with
MitoQ
or
Idb
then
exposed
to
menadione
(MN)
simultaneous
treatment.
Mitochondrial
parameters
evaluated
through
adenosine
triphosphate
viability
assays,
JC-1
staining
for
membrane
potential,
Tom-20
antibody
fragmentation,
analysis
performed
ImageJ
software.
HCEnC-21T
additionally
ultraviolet-A
(25
J/cm
2
)
assess
drug
effects
under
physiological
stress.
fragmentation
FECD
specimens
was
analyzed
pre-
post-treatment
drugs.
Statistical
1-/2-way
variance
post-hoc
Tukey
test.
Results:
enhanced
cell
potential
both
MN-induced
reduced
by
32%
more
than
13%
SVF5-54F
cells.
Under
stress,
improved
function
31%
25%,
respectively,
increasing
42%
specimens.
Conclusions:
Differential
responses
across
lines
highlight
disease
heterogeneity.
protected
CEnCs
from
oxidative
stress
bioenergetics,
suggesting
that
antioxidants
could
be
considered
CEnCs.
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.
Frontiers in Pharmacology,
Journal Year:
2025,
Volume and Issue:
16
Published: April 16, 2025
Diabetes
mellitus
(DM)
is
a
chronic
metabolic
disorder
marked
by
sustained
hyperglycemia.
These
disturbances
contribute
to
extensive
damage
across
various
tissues
and
organs,
giving
rise
severe
complications
such
as
vision
loss,
kidney
failure,
amputations,
higher
morbidity
mortality
rates.
Furthermore,
DM
imposes
substantial
economic
emotional
burden
on
patients,
families,
healthcare
systems.
Mitophagy,
selective
process
that
targets
the
clearance
of
damaged
or
dysfunctional
mitochondria,
pivotal
for
sustaining
cellular
homeostasis
through
mitochondrial
turnover
recycling.
Emerging
evidence
indicates
mitophagy
acts
key
pathogenic
driver
in
pathogenesis
its
associated
complications.
Natural
small
molecules
are
particularly
attractive
this
regard,
offering
advantages
low
toxicity,
favorable
pharmacokinetic
profiles,
excellent
biocompatibility,
broad
range
biochemical
activities.
This
review
systematically
evaluates
mechanistic
roles
natural
molecules-including
ginsenosides,
resveratrol,
berberine-in
enhancing
restoring
via
activation
core
signaling
pathways
(e.g.,
PINK1/Parkin,
BNIP3/NIX,
FUNDC1).
collectively
ameliorate
pathological
hallmarks
DM,
oxidative
stress,
inflammation,
insulin
resistance.
integration
nanotechnology
with
these
compounds
optimizes
their
bioavailability
tissue-specific
targeting,
thereby
establishing
transformative
therapeutic
platform
management.
Current
demonstrates
modulation
not
only
offers
novel
strategies
but
also
advances
foundation
future
drug
development
targeting
disorders.