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.
Cell Death and Differentiation,
Journal Year:
2014,
Volume and Issue:
22(3), P. 377 - 388
Published: Sept. 26, 2014
Autophagy
is
a
catabolic
process
aimed
at
recycling
cellular
components
and
damaged
organelles
in
response
to
diverse
conditions
of
stress,
such
as
nutrient
deprivation,
viral
infection
genotoxic
stress.
A
growing
amount
evidence
recent
years
argues
for
oxidative
stress
acting
the
converging
point
these
stimuli,
with
reactive
oxygen
species
(ROS)
nitrogen
(RNS)
being
among
main
intracellular
signal
transducers
sustaining
autophagy.
This
review
aims
providing
novel
insight
into
regulatory
pathways
autophagy
glucose
amino
acid
well
their
tight
interconnection
metabolic
networks
redox
homeostasis.
The
role
nitrosative
also
discussed
light
its
harmful
both
biomolecules
mediator
through
reversible
posttranslational
modifications
thiol-containing
proteins.
redox-independent
relationship
between
antioxidant
response,
occurring
p62/Keap1/Nrf2
pathway,
addressed
order
provide
wide
perspective
upon
Herein,
we
attempt
afford
an
overview
complex
crosstalk
DNA
damage
(DDR),
focusing
on
activated
ROS
RNS
overproduction.
Along
lines,
direct
indirect
DDR
dissected
depth.
Molecular Cancer,
Journal Year:
2015,
Volume and Issue:
14(1)
Published: Feb. 20, 2015
Metastasis
is
a
crucial
hallmark
of
cancer
progression,
which
involves
numerous
factors
including
the
degradation
extracellular
matrix
(ECM),
epithelial-to-mesenchymal
transition
(EMT),
tumor
angiogenesis,
development
an
inflammatory
microenvironment,
and
defects
in
programmed
cell
death.
Programmed
death,
such
as
apoptosis,
autophagy,
necroptosis,
plays
roles
metastatic
processes.
Malignant
cells
must
overcome
these
various
forms
death
to
metastasize.
This
review
summarizes
recent
advances
understanding
mechanisms
by
key
regulators
necroptosis
participate
metastasis
discusses
crosstalk
between
involved
regulation
metastasis.
Signal Transduction and Targeted Therapy,
Journal Year:
2021,
Volume and Issue:
6(1)
Published: Feb. 3, 2021
Abstract
Ferroptosis
is
an
iron-dependent
cell
death,
which
different
from
apoptosis,
necrosis,
autophagy,
and
other
forms
of
death.
The
process
ferroptotic
death
defined
by
the
accumulation
lethal
lipid
species
derived
peroxidation
lipids,
can
be
prevented
iron
chelators
(e.g.,
deferiprone,
deferoxamine)
small
lipophilic
antioxidants
ferrostatin,
liproxstatin).
This
review
summarizes
current
knowledge
about
regulatory
mechanism
ferroptosis
its
association
with
several
pathways,
including
iron,
lipid,
cysteine
metabolism.
We
have
further
discussed
contribution
to
pathogenesis
diseases
such
as
cancer,
ischemia/reperfusion,
various
neurodegenerative
Alzheimer’s
disease
Parkinson’s
disease),
evaluated
therapeutic
applications
inhibitors
in
clinics.
Cell Death and Differentiation,
Journal Year:
2014,
Volume and Issue:
22(1), P. 58 - 73
Published: Sept. 19, 2014
Cells
exposed
to
extreme
physicochemical
or
mechanical
stimuli
die
in
an
uncontrollable
manner,
as
a
result
of
their
immediate
structural
breakdown.
Such
unavoidable
variant
cellular
demise
is
generally
referred
'accidental
cell
death'
(ACD).
In
most
settings,
however,
death
initiated
by
genetically
encoded
apparatus,
correlating
with
the
fact
that
its
course
can
be
altered
pharmacologic
genetic
interventions.
'Regulated
(RCD)
occur
part
physiologic
programs
activated
once
adaptive
responses
perturbations
extracellular
intracellular
microenvironment
fail.
The
biochemical
phenomena
accompany
RCD
may
harnessed
classify
it
into
few
subtypes,
which
often
(but
not
always)
exhibit
stereotyped
morphologic
features.
Nonetheless,
efficiently
inhibiting
processes
are
commonly
thought
cause
RCD,
such
activation
executioner
caspases
apoptosis,
does
exert
true
cytoprotective
effects
mammalian
system,
but
simply
alters
kinetics
shifts
and
correlates.
Conversely,
bona
fide
cytoprotection
achieved
transduction
lethal
signals
early
phases
process,
when
still
operational.
Thus,
mechanisms
truly
execute
less
understood,
inhibitable
perhaps
more
homogeneous
than
previously
thought.
Here,
Nomenclature
Committee
on
Cell
Death
formulates
set
recommendations
help
scientists
researchers
discriminate
between
essential
accessory
aspects
death.
Molecular Cancer,
Journal Year:
2019,
Volume and Issue:
18(1)
Published: May 23, 2019
Apoptosis
resistance
is
to
a
large
extent
major
obstacle
leading
chemotherapy
failure
during
cancer
treatment.
Bypassing
the
apoptotic
pathway
induce
cell
death
considered
be
promising
approach
overcoming
this
problem.
Necroptosis
regulated
necrotic
modality
in
caspase-independent
fashion
and
mainly
mediated
by
Receptor-Interacting
Protein
1
(RIP1),
RIP3,
Mixed
Lineage
Kinase
Domain-Like
(MLKL).
serves
as
an
alternative
mode
of
programmed
apoptosis
may
trigger
amplify
antitumor
immunity
therapy.
The
role
necroptosis
complicated.
expression
key
regulators
necroptotic
generally
downregulated
cells,
suggesting
that
cells
also
evade
survive;
however,
certain
types
cancer,
level
mediators
elevated.
can
elicit
strong
adaptive
immune
responses
defend
against
tumor
progression;
recruited
inflammatory
response
promote
tumorigenesis
metastasis,
generate
immunosuppressive
microenvironment.
reportedly
promotes
oncogenesis
metastasis
despite
evidence
demonstrating
its
antimetastatic
cancer.
In
addition,
microenvironments
direct
lineage
commitment
determine
subtype
development
liver
A
plethora
compounds
drugs
targeting
exhibit
potential
efficacy,
but
their
clinical
feasibility
must
validated.
Better
knowledge
mechanism
physiological
pathological
functions
urgently
required
solve
remaining
mysteries
surrounding
review,
we
briefly
introduce
molecular
characteristics
necroptosis,
interplay
between
other
mechanisms,
crosstalk
metabolic
signaling
detection
methods.
We
summarize
intricate
progression,
prognosis
patients,
regulation,
determination
therapeutics.