Aging Cell,
Journal Year:
2020,
Volume and Issue:
19(4)
Published: April 1, 2020
Abstract
One
of
the
key
mechanisms
underlying
skeletal
muscle
functional
deterioration
during
aging
is
disrupted
mitochondrial
dynamics.
Regulation
dynamics
essential
to
maintain
a
healthy
population
and
prevent
accumulation
damaged
mitochondria;
however,
regulatory
are
poorly
understood.
We
demonstrated
loss
content
in
concomitant
with
dysregulation
miR‐181a
target
interactions.
Using
approaches
mito‐QC
assay,
we
have
established
that
an
endogenous
regulator
through
concerted
regulation
Park2,
p62/SQSTM1,
DJ‐1
vitro.
Downregulation
age
was
associated
autophagy‐related
proteins
abnormal
mitochondria.
Restoring
levels
old
mice
prevented
p62,
DJ‐1,
PARK2,
improved
quality
function.
These
results
provide
physiological
evidence
for
potential
microRNA‐based
interventions
age‐related
atrophy
wider
significance
diseases
Cellular and Molecular Neurobiology,
Journal Year:
2023,
Volume and Issue:
43(7), P. 3265 - 3276
Published: July 1, 2023
The
retinal
pigment
epithelium
(RPE)
is
a
highly
specialized
and
polarized
epithelial
cell
layer
that
plays
an
important
role
in
sustaining
the
structural
functional
integrity
of
photoreceptors.
However,
death
RPE
common
pathological
feature
various
diseases,
especially
age-related
macular
degeneration
(AMD)
diabetic
retinopathy
(DR).
Mitophagy,
as
programmed
self-degradation
dysfunctional
mitochondria,
crucial
for
maintaining
cellular
homeostasis
survival
under
stress.
contains
high
density
mitochondria
necessary
it
to
meet
energy
demands,
so
severe
stimuli
can
cause
mitochondrial
dysfunction
excess
generation
intracellular
reactive
oxygen
species
(ROS),
which
further
trigger
oxidative
stress-involved
mitophagy.
In
this
review,
we
summarize
classical
pathways
mitophagy
investigate
its
progression
aiming
provide
new
therapeutic
strategy
treating
degenerative
diseases.
AMD
DR.
AMD,
excessive
ROS
production
promotes
by
activating
Nrf2/p62
pathway,
while
DR,
may
suppress
FOXO3-PINK1/parkin
signaling
pathway
or
TXNIP-mitochondria-lysosome-mediated
Antioxidants,
Journal Year:
2023,
Volume and Issue:
12(2), P. 480 - 480
Published: Feb. 14, 2023
The
mitochondrion
is
also
a
major
site
for
maintaining
redox
homeostasis
between
reactive
oxygen
species
(ROS)
generation
and
scavenging.
quantity,
quality,
functional
integrity
of
mitochondria
are
crucial
regulating
intracellular
the
normal
physiological
function
cells.
role
oxidative
stress
in
human
disease
well
established,
particularly
inflammatory
bowel
gastrointestinal
mucosal
diseases.
Oxidative
could
result
from
an
imbalance
ROS
antioxidative
system.
Mitochondria
both
main
sites
production
target
ROS.
It
vicious
cycle
which
initial
ROS-induced
mitochondrial
damage
enhanced
that,
turn,
leads
to
further
eventually
massive
intestinal
cell
death.
can
be
significantly
mitigated
by
mitophagy,
clears
damaged
mitochondria.
In
this
review,
we
aimed
review
molecular
mechanisms
involved
regulation
mitophagy
their
relationship
some
We
believe
reviews
provide
new
ideas
scientific
basis
researching
antioxidants
preventing
diseases
related
damage.
Cells,
Journal Year:
2019,
Volume and Issue:
8(9), P. 973 - 973
Published: Aug. 25, 2019
Since
their
initial
discovery
around
two
decades
ago,
the
yeast
autophagy-related
(Atg)8
protein
and
its
mammalian
homologues
of
light
chain
3
(LC3)
γ-aminobutyric
acid
receptor
associated
proteins
(GABARAP)
families
have
been
key
for
tremendous
expansion
our
knowledge
about
autophagy,
a
process
in
which
cytoplasmic
material
become
targeted
lysosomal
degradation.
These
are
ubiquitin-like
that
directly
conjugated
to
lipid
autophagy
membrane
upon
induction
thus
providing
marker
pathway,
allowing
studies
autophagosome
biogenesis
maturation.
Moreover,
ATG8
function
recruit
components
core
machinery
as
well
cargo
selective
Importantly,
comprehensive
structural
biochemical
vitro
required
lipidation,
genetic
manipulation
various
model
organisms,
provided
novel
insight
into
molecular
mechanisms
pathophysiological
roles
mATG8
proteins.
Recently,
it
has
evident
conjugation
also
involved
intracellular
pathways
processes
not
related
autophagy.
This
review
focuses
on
functions
other
pathways,
links
disease.
Aging Cell,
Journal Year:
2020,
Volume and Issue:
19(4)
Published: April 1, 2020
Abstract
One
of
the
key
mechanisms
underlying
skeletal
muscle
functional
deterioration
during
aging
is
disrupted
mitochondrial
dynamics.
Regulation
dynamics
essential
to
maintain
a
healthy
population
and
prevent
accumulation
damaged
mitochondria;
however,
regulatory
are
poorly
understood.
We
demonstrated
loss
content
in
concomitant
with
dysregulation
miR‐181a
target
interactions.
Using
approaches
mito‐QC
assay,
we
have
established
that
an
endogenous
regulator
through
concerted
regulation
Park2,
p62/SQSTM1,
DJ‐1
vitro.
Downregulation
age
was
associated
autophagy‐related
proteins
abnormal
mitochondria.
Restoring
levels
old
mice
prevented
p62,
DJ‐1,
PARK2,
improved
quality
function.
These
results
provide
physiological
evidence
for
potential
microRNA‐based
interventions
age‐related
atrophy
wider
significance
diseases
