International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
26(1), P. 57 - 57
Published: Dec. 25, 2024
As
the
organism
ages,
there
is
a
decline
in
effective
energy
supply,
and
this
retards
ability
to
elaborate
new
proteins.
The
consequences
of
are
especially
marked
gradual
brain
function.
senescence
cells
their
constituent
organelles
ultimately
cause
aging
entire
nervous
system.
What
less
immediately
obvious
that
also
accompanied
by
failure
catabolic
events
lead
removal
non-functional
ineffective
subcellular
components.
non-working
cellular
elements
within
essential
order
allow
appearance
fresh
with
full
range
capacities.
Thus,
maintenance
operative
mechanisms
for
dispersal
failed
tissue
components
important,
its
diminished
capacity
significant
contributory
factor
onset
progression
age-related
neurological
disorder.
This
report
discusses
underlying
autophagy
phagocytosis
how
these
can
be
adversely
modulated
as
proceeds.
means
which
recycling
may
reinstated
aged
considered.
The Journal of Cell Biology,
Journal Year:
2025,
Volume and Issue:
224(5)
Published: March 7, 2025
We
here
identify
the
endosomal
protein
SNX10
as
a
negative
regulator
of
piecemeal
mitophagy
OXPHOS
machinery
components.
In
control
conditions,
localizes
to
early
endocytic
compartments
in
PtdIns3P-dependent
manner
and
modulates
trafficking
but
also
shows
dynamic
connections
with
mitochondria.
Upon
hypoxia-mimicking
late
structures
containing
selected
mitochondrial
proteins,
including
COX-IV
SAMM50,
autophagy
proteins
SQSTM1/p62
LC3B.
The
turnover
was
enhanced
SNX10-depleted
cells,
corresponding
reduced
respiration
citrate
synthase
activity.
Importantly,
zebrafish
larvae
lacking
Snx10
show
levels
Cox-IV,
well
elevated
ROS
ROS-mediated
cell
death
brain,
demonstrating
vivo
relevance
SNX10-mediated
modulation
bioenergetics.
Lipids in Health and Disease,
Journal Year:
2024,
Volume and Issue:
23(1)
Published: July 19, 2024
Abstract
Lipid
droplets
(LDs),
which
are
active
organelles,
derive
from
the
monolayer
membrane
of
endoplasmic
reticulum
and
encapsulate
neutral
lipids
internally.
LD-associated
proteins
like
RAB,
those
in
PLIN
family,
CIDE
family
participate
LD
formation
development,
they
players
various
diseases,
metabolic
processes
(i.e.,
obesity,
non-alcoholic
fatty
liver
disease,
autophagy).
Our
synthesis
on
existing
research
includes
insights
LDs
to
their
mechanisms
action,
provide
an
overview
needed
for
advancing
into
diseases
lipid
metabolism.
Intensive Care Medicine Experimental,
Journal Year:
2025,
Volume and Issue:
13(1)
Published: Feb. 18, 2025
Abstract
Sepsis
is
a
life-threatening
multi-organ
dysfunction
syndrome
caused
by
dysregulated
host
response
to
infection,
posing
significant
global
healthcare
challenge.
Sepsis-induced
myocardial
(SIMD)
common
complication
of
sepsis,
significantly
increasing
mortality
due
its
high
energy
demands
and
low
compensatory
reserves.
The
substantial
mitochondrial
damage
rather
than
cell
apoptosis
in
SIMD
suggests
disrupted
cardiac
metabolism
as
crucial
pathophysiological
mechanism.
Therefore,
we
systematically
reviewed
the
mechanisms
underlying
SIMD,
including
alterations
substrates,
excitation–contraction
coupling
processes,
dysfunction,
autophagy
biogenesis,
summarizing
potential
therapeutic
targets
within
them.
The Journal of Immunology,
Journal Year:
2025,
Volume and Issue:
unknown
Published: May 16, 2025
Abstract
Toll-interacting
protein
(Tollip)
is
an
intracellular
adaptor
with
diverse
functions
including
regulation
of
autophagy
mitochondria—mitophagy.
Tollip
deficiency
promotes
viral
infection,
but
whether
mitophagy
involved
remains
unclear.
We
sought
to
determine
if
and
associated
signaling
such
as
mitochondrial
DNA
(mtDNA)
release
activation
stimulator
interferon
genes
(STING)
contribute
worsened
infection
due
deficiency.
Wild-type
knockout
(KO)
C57/BL6
mice
were
intranasally
infected
influenza
A
virus
(IAV),
then
treated
or
without
a
STING
agonist
2′3′cGAMP
for
4
d.
PINK1
(an
initiator
mitophagy)
KO
mouse
tracheal
epithelial
cells
(mTECs)
IAV
reveal
the
role
in
infection.
In
IAV-infected
mice,
enhanced
lung
(more
BNIP3L,
less
p62),
decreased
mtDNA.
Furthermore,
suppressed
antiviral
response
(eg
IFN-β
MX1),
increased
load.
activated
coupled
virus.
PINK1-deficient
mtDNA
augmented
responses.
mTECs
significantly
Our
findings
suggest
that
reduces
during
resulting
Reduction
and/or
may
open
novel
avenues
therapeutic
intervention
human
subjects
ACS Pharmacology & Translational Science,
Journal Year:
2024,
Volume and Issue:
7(11), P. 3540 - 3558
Published: Oct. 15, 2024
Urolithin
A
(UA)
has
demonstrated
the
ability
to
stimulate
mitophagy
and
enhance
mitochondrial
cellular
health
in
skeletal
muscles
humans
after
oral
administration.
It
is
hypothesized
that
targeted
delivery
of
UA
as
inhaled
dry
powders
lungs
will
through
biogenesis.
This
study
aimed
engineer
inhalable
excipient-free
powder
inhalers
(DPIs)
for
pulmonary
delivery.
The
particles
were
designed
by
particle
engineering
from
dilute
organic
solutions
using
state-of-the-art
spray
drying
technology
a
closed
mode.
Comprehensive
physicochemical
characterization
advanced
microscopy
techniques
conducted
examine
phase
behavior,
molecular
properties,
which
are
necessary
rational
design
inhalation
aerosols.
Molecular
fingerprinting
was
attenuated
total
reflectance-Fourier
transform
infrared
(ATR-FTIR)
spectroscopy
Raman
spectroscopy.
Chemical
imaging
mapping
confocal
(CRM)
IR
microscopy.
spray-dried
(SD)
successfully
produced
at
different
spraying
pump
feed
rates
exhibited
favorable
properties.
SD
outstanding
vitro
aerosol
dispersion
performance
with
an
FDI-approved
human
DPI
device
(Neohaler)
correlated
rate.
In
