Essays in Biochemistry,
Journal Year:
2017,
Volume and Issue:
61(6), P. 733 - 749
Published: Dec. 12, 2017
The
lysosome
plays
a
pivotal
role
between
catabolic
and
anabolic
processes
as
the
nexus
for
signalling
pathways
responsive
to
variety
of
factors,
such
growth,
nutrient
availability,
energetic
status
cellular
stressors.
Lysosomes
are
also
terminal
degradative
organelles
autophagy
through
which
macromolecules
damaged
components
degraded.
Autophagy
acts
homeostatic
pathway
that
is
essential
organismal
physiology.
Decline
in
during
ageing
or
many
diseases,
including
late-onset
forms
neurodegeneration
considered
major
contributing
factor
pathology.
Multiple
lines
evidence
indicate
impairment
central
mechanism
underlying
several
lysosomal
storage
disorders
(LSDs).
LSDs
class
rare,
inherited
whose
histopathological
hallmark
accumulation
undegraded
materials
lysosomes
due
abnormal
function.
Inefficient
capability
has
negative
impact
on
flux
autophagic
pathway,
therefore
dysregulated
emerging
relevant
disease
mechanism.
Pathology
generally
early-onset,
severe
life-limiting
but
current
therapies
limited
absent;
recognizing
common
defects
raises
new
possibilities
therapy.
In
this
review,
we
describe
mechanisms
by
occur,
focusing
perturbations
present
latest
data
supporting
development
novel
therapeutic
approaches
related
modulation
autophagy.
Autophagy,
Journal Year:
2021,
Volume and Issue:
17(1), P. 1 - 382
Published: Jan. 2, 2021
In
2008,
we
published
the
first
set
of
guidelines
for
standardizing
research
in
autophagy.
Since
then,
this
topic
has
received
increasing
attention,
and
many
scientists
have
entered
field.
Our
knowledge
base
relevant
new
technologies
also
been
expanding.
Thus,
it
is
important
to
formulate
on
a
regular
basis
updated
monitoring
autophagy
different
organisms.
Despite
numerous
reviews,
there
continues
be
confusion
regarding
acceptable
methods
evaluate
autophagy,
especially
multicellular
eukaryotes.
Here,
present
investigators
select
interpret
examine
related
processes,
reviewers
provide
realistic
reasonable
critiques
reports
that
are
focused
these
processes.
These
not
meant
dogmatic
rules,
because
appropriateness
any
assay
largely
depends
question
being
asked
system
used.
Moreover,
no
individual
perfect
every
situation,
calling
use
multiple
techniques
properly
monitor
each
experimental
setting.
Finally,
several
core
components
machinery
implicated
distinct
autophagic
processes
(canonical
noncanonical
autophagy),
implying
genetic
approaches
block
should
rely
targeting
two
or
more
autophagy-related
genes
ideally
participate
steps
pathway.
Along
similar
lines,
proteins
involved
regulate
other
cellular
pathways
including
apoptosis,
all
them
can
used
as
specific
marker
bona
fide
responses.
critically
discuss
current
assessing
information
they
can,
cannot,
provide.
ultimate
goal
encourage
intellectual
technical
innovation
Journal of Clinical Investigation,
Journal Year:
2015,
Volume and Issue:
125(1), P. 14 - 24
Published: Jan. 1, 2015
Defects
in
autophagy
have
been
linked
to
a
wide
range
of
medical
illnesses,
including
cancer
as
well
infectious,
neurodegenerative,
inflammatory,
and
metabolic
diseases.
These
observations
led
the
hypothesis
that
inducers
may
prevent
or
treat
certain
clinical
conditions.
Lifestyle
nutritional
factors,
such
exercise
caloric
restriction,
exert
their
known
health
benefits
through
pathway.
Several
currently
available
FDA-approved
drugs
shown
enhance
autophagy,
this
autophagy-enhancing
action
be
repurposed
for
use
novel
indications.
The
development
new
are
designed
more
selective
function
target
organs
is
expected
maximize
while
minimizing
toxicity.
This
Review
summarizes
rationale
current
approaches
developing
medicine,
factors
considered
defining
disease
targets
therapy,
potential
treatment
human
health.
Journal of Molecular Biology,
Journal Year:
2019,
Volume and Issue:
432(8), P. 2462 - 2482
Published: Nov. 2, 2019
Macroautophagy
is
a
conserved
catabolic
process
observed
in
all
eukaryotic
cells,
during
which
selected
cellular
components
are
transported
to
and
broken
down
within
lysosomes.
The
starts
with
the
capture
of
unnecessary
material
into
autophagosomes,
followed
by
autophagosome-lysosome
fusion
generate
autolysosomes
that
degrade
cargo.
In
past
quarter-century,
our
knowledge
about
autophagosome
formation
almost
exponentially
increased,
while
later
steps
were
much
less
studied.
This
fortunately
changed
few
years,
more
publications
focusing
on
fate
completed
autophagosome.
this
review,
we
aspire
summarize
current
molecular
mechanisms
fusion.
Cells,
Journal Year:
2019,
Volume and Issue:
8(7), P. 674 - 674
Published: July 3, 2019
Autophagy
(self-eating)
is
a
conserved
cellular
degradation
process
that
plays
important
roles
in
maintaining
homeostasis
and
preventing
nutritional,
metabolic,
infection-mediated
stresses.
dysfunction
can
have
various
pathological
consequences,
including
tumor
progression,
pathogen
hyper-virulence,
neurodegeneration.
This
review
describes
the
mechanisms
of
autophagy
its
associations
with
other
cell
death
mechanisms,
apoptosis,
necrosis,
necroptosis,
autosis.
has
both
positive
negative
infection,
cancer,
neural
development,
metabolism,
cardiovascular
health,
immunity,
iron
homeostasis.
Genetic
defects
such
as
static
childhood
encephalopathy
neurodegeneration
adulthood,
Crohn’s
disease,
hereditary
spastic
paraparesis,
Danon
X-linked
myopathy
excessive
autophagy,
sporadic
inclusion
body
myositis.
Further
studies
on
different
microbial
infections
could
help
to
design
develop
novel
therapeutic
strategies
against
pathogenic
microbes.
progress
prospects
research
activators
suppressors,
which
be
used
intervention
numerous
diseases
drugs
protect
human
animal
health.
AJP Cell Physiology,
Journal Year:
2015,
Volume and Issue:
308(9), P. C710 - C719
Published: Feb. 12, 2015
Regular
exercise
leads
to
systemic
metabolic
benefits,
which
require
remodeling
of
energy
resources
in
skeletal
muscle.
During
acute
exercise,
the
increase
demands
initiate
mitochondrial
biogenesis,
orchestrated
by
transcriptional
coactivator
peroxisome
proliferator-activated
receptor-γ
coactivator-1α
(PGC-1α).
Much
less
is
known
about
degradation
mitochondria
following
although
new
evidence
implicates
a
cellular
recycling
mechanism,
autophagy/mitophagy,
exercise-induced
adaptations.
How
mitophagy
activated
and
what
role
PGC-1α
plays
this
process
during
have
yet
be
evaluated.
Thus
we
investigated
autophagy/mitophagy
muscle
immediately
an
bout
or
90
min
wild-type
(WT)
knockout
(KO)
animals.
Deletion
resulted
40%
decrease
content,
as
well
25%
decline
running
performance,
was
accompanied
severe
acidosis
KO
animals,
indicating
distress.
Exercise
induced
significant
increases
gene
transcripts
various
(e.g.,
cytochrome
oxidase
subunit
IV
transcription
factor
A)
autophagy-related
p62
light
chain
3)
genes
WT,
but
not
KO,
also
enhanced
targeting
for
mitophagy,
increased
autophagy
flux,
WT
This
effect
attenuated
absence
PGC-1α.
We
identified
Niemann-Pick
C1,
transmembrane
protein
involved
lysosomal
lipid
trafficking,
target
that
with
exercise.
These
results
suggest
turnover
at
least
part
coordinated
Anna
Vainshtein
received
AJP-Cell
2015
Paper
Year
award.
Listen
podcast
coauthor
David
A.
Hood
http://ajpcell.podbean.com/e/ajp-cell-paper-of-the-year-2015-award-podcast/
.