Annual Review of Immunology,
Journal Year:
2017,
Volume and Issue:
36(1), P. 73 - 101
Published: Nov. 16, 2017
The
cellular
degradative
pathway
of
autophagy
has
a
fundamental
role
in
immunity.
Here,
we
review
the
function
and
proteins
inflammation.
We
discuss
how
machinery
controls
burden
infectious
agents
while
simultaneously
limiting
inflammatory
pathologies,
which
often
involves
processes
that
are
distinct
from
conventional
autophagy.
Among
newly
emerging
describe
LC3-associated
phagocytosis
targeting
by
proteins,
both
require
many
same
mediate
also
contributes
to
differentiation
myeloid
lymphoid
cell
types,
coordinates
multicellular
immunity,
facilitates
memory
responses.
Together,
these
functions
establish
an
intimate
link
between
autophagy,
mucosal
chronic
diseases.
Finally,
offer
our
perspective
on
current
challenges
barriers
translation.
Circulation Research,
Journal Year:
2017,
Volume and Issue:
120(11), P. 1812 - 1824
Published: May 25, 2017
Autophagy
contributes
to
the
maintenance
of
intracellular
homeostasis
in
most
cells
cardiovascular
origin,
including
cardiomyocytes,
endothelial
cells,
and
arterial
smooth
muscle
cells.
Mitophagy
is
an
autophagic
response
that
specifically
targets
damaged,
hence
potentially
cytotoxic,
mitochondria.
As
these
organelles
occupy
a
critical
position
bioenergetics
system,
mitophagy
particularly
important
for
health
disease.
Consistent
with
this
notion,
genetic
defects
autophagy
or
have
been
shown
exacerbate
propensity
laboratory
animals
spontaneously
develop
cardiodegenerative
disorders.
Moreover,
pharmacological
maneuvers
alter
mitophagic
flux
influence
disease
outcome
rodent
models
several
conditions,
such
as
myocardial
infarction,
various
types
cardiomyopathy,
atherosclerosis.
In
review,
we
discuss
intimate
connection
between
autophagy,
mitophagy,
Science,
Journal Year:
2014,
Volume and Issue:
345(6203)
Published: Sept. 18, 2014
Beyond
their
contribution
to
basic
metabolism,
the
major
cellular
organelles,
in
particular
mitochondria,
can
determine
whether
cells
respond
stress
an
adaptive
or
suicidal
manner.
Thus,
mitochondria
continuously
adapt
shape
changing
bioenergetic
demands
as
they
are
subjected
quality
control
by
autophagy,
undergo
a
lethal
permeabilization
process
that
initiates
apoptosis.
Along
similar
lines,
multiple
proteins
involved
metabolic
circuitries,
including
oxidative
phosphorylation
and
transport
of
metabolites
across
membranes,
may
participate
regulated
catastrophic
dismantling
organelles.
Many
factors
were
initially
characterized
cell
death
regulators
now
known
physically
functionally
interact
with
enzymes.
several
cues
regulate
propensity
activate
self-destructive
programs,
part
acting
on
nutrient
sensors.
This
suggests
existence
"metabolic
checkpoints"
dictate
fate
response
fluctuations.
Here,
we
discuss
recent
insights
into
intersection
between
metabolism
regulation
have
implications
for
comprehension
manipulation
unwarranted
loss.
Microbial Cell,
Journal Year:
2016,
Volume and Issue:
3(12), P. 588 - 596
Published: Dec. 1, 2016
Macroautophagy/autophagy
is
an
evolutionarily
conserved
cellular
degradation
process
that
targets
cytoplasmic
materials
including
cytosol,
macromolecules
and
unwanted
organelles.
The
discovery
analysis
of
autophagy-related
(Atg)
proteins
have
unveiled
much
the
machinery
autophagosome
formation.
Although
initially
autophagy
was
regarded
as
a
survival
response
to
stress,
recent
studies
revealed
its
significance
in
organismal
homeostasis,
development
immunity.
Autophagic
dysfunction
dysregulation
are
implicated
various
diseases.
In
this
review,
we
briefly
summarize
physiological
roles,
molecular
mechanism,
regulatory
network,
pathophysiological
roles
autophagy.
Journal of Pineal Research,
Journal Year:
2015,
Volume and Issue:
59(3), P. 292 - 307
Published: July 22, 2015
Endoplasmic
reticulum
(ER)
is
a
dynamic
organelle
that
participates
in
number
of
cellular
functions
by
controlling
lipid
metabolism,
calcium
stores,
and
proteostasis.
Under
stressful
situations,
the
ER
environment
compromised,
protein
maturation
impaired;
this
causes
misfolded
proteins
to
accumulate
characteristic
stress
response
named
unfolded
(UPR).
UPR
protects
cells
from
contributes
homeostasis
re-establishment;
however,
during
prolonged
stress,
activation
promotes
cell
death.
stressors
can
modulate
autophagy
which
turn,
depending
situation,
induces
survival
or
Interactions
different
autophagy-
apoptosis-related
also
common
signaling
pathways
have
been
found,
suggesting
an
interplay
between
these
processes,
although
their
features
are
still
unknown.
A
pathologies
including
metabolic,
neurodegenerative
cardiovascular
diseases,
cancer,
inflammation,
viral
infections
associated
with
leading
growing
interest
targeting
components
as
therapeutic
strategy.
Melatonin
has
variety
antioxidant,
anti-inflammatory,
antitumor
effects.
As
such,
it
modulates
apoptosis
cancer
cells,
neurodegeneration
development
liver
diseases
well
other
pathologies.
Here,
we
review
effects
melatonin
on
main
mechanisms,
focusing
its
ability
regulate
autophagic
apoptotic
processes.
studies
analyzed
modulation
indole
remains
limited,
further
research
necessary
for
better
understanding
crosstalk
autophagy,
clearly
delineate
mechanisms
responses.
International Journal of Molecular Sciences,
Journal Year:
2017,
Volume and Issue:
18(2), P. 367 - 367
Published: Feb. 10, 2017
Non-small-cell
lung
cancer
(NSCLC)
constitutes
85%
of
all
cancers,
and
is
the
leading
cause
cancer-related
death
worldwide.
The
poor
prognosis
resistance
to
both
radiation
chemotherapy
warrant
further
investigation
into
molecular
mechanisms
NSCLC
development
new,
more
efficacious
therapeutics.
processes
autophagy
apoptosis,
which
induce
degradation
proteins
organelles
or
cell
upon
cellular
stress,
are
crucial
in
pathophysiology
NSCLC.
close
interplay
between
apoptosis
through
shared
signaling
pathways
complicates
our
understanding
how
regulated.
apoptotic
effect
controversial
as
inhibitory
stimulatory
effects
have
been
reported
In
addition,
crosstalk
regulating
exists.
Here,
we
review
recent
advances
relationship
NSCLC,
aiming
provide
few
insights
discovery
novel
pathogenic
factors
new
