Experimental & Molecular Medicine,
Journal Year:
2023,
Volume and Issue:
55(8), P. 1595 - 1619
Published: Aug. 23, 2023
Abstract
Mitochondria,
ubiquitous
double-membrane-bound
organelles,
regulate
energy
production,
support
cellular
activities,
harbor
metabolic
pathways,
and,
paradoxically,
mediate
cell
fate.
Evidence
has
shown
mitochondria
as
points
of
convergence
for
diverse
death-inducing
pathways
that
trigger
the
various
mechanisms
underlying
apoptotic
and
nonapoptotic
programmed
death.
Thus,
dysfunctional
eventually
lead
or
contribute
to
age-related
diseases,
such
neurodegenerative,
cardiovascular
diseases.
mitochondrion-associated
death-based
treatments
show
great
therapeutic
potential,
providing
novel
insights
in
clinical
trials.
This
review
discusses
mitochondrial
quality
control
networks
with
activity
triggered
by
stimuli
maintain
homeostasis
via
mitohormesis,
unfolded
protein
response,
mitophagy.
The
also
presents
details
on
forms
mitochondria-associated
death,
including
apoptosis,
necroptosis,
ferroptosis,
pyroptosis,
parthanatos,
paraptosis,
highlights
their
involvement
disease
pathogenesis,
collectively
suggesting
directions
further
research.
European Journal of Immunology,
Journal Year:
2019,
Volume and Issue:
49(10), P. 1457 - 1973
Published: Oct. 1, 2019
These
guidelines
are
a
consensus
work
of
considerable
number
members
the
immunology
and
flow
cytometry
community.
They
provide
theory
key
practical
aspects
enabling
immunologists
to
avoid
common
errors
that
often
undermine
immunological
data.
Notably,
there
comprehensive
sections
all
major
immune
cell
types
with
helpful
Tables
detailing
phenotypes
in
murine
human
cells.
The
latest
techniques
applications
also
described,
featuring
examples
data
can
be
generated
and,
importantly,
how
analysed.
Furthermore,
tips,
tricks
pitfalls
avoid,
written
peer-reviewed
by
leading
experts
field,
making
this
an
essential
research
companion.
Redox Biology,
Journal Year:
2020,
Volume and Issue:
37, P. 101799 - 101799
Published: Oct. 1, 2020
Oxidative
stress,
a
cytopathic
outcome
of
excessive
generation
ROS
and
the
repression
antioxidant
defense
system
for
elimination,
is
involved
in
pathogenesis
multiple
diseases,
including
diabetes
its
complications.
Retinopathy,
microvascular
complication
diabetes,
primary
cause
acquired
blindness
diabetic
patients.
stress
has
been
verified
as
one
critical
contributor
to
retinopathy.
can
both
contribute
result
from
metabolic
abnormalities
induced
by
hyperglycemia,
mainly
increased
flux
polyol
pathway
hexosamine
pathway,
hyper-activation
protein
kinase
C
(PKC)
isoforms,
accumulation
advanced
glycation
end
products
(AGEs).
Moreover,
hyperglycemia-mediated
epigenetic
modification
also
leads
imbalance
between
scavenging
production
ROS.
Excessive
induces
mitochondrial
damage,
cellular
apoptosis,
inflammation,
lipid
peroxidation,
structural
functional
alterations
retina.
Therefore,
it
important
understand
elucidate
oxidative
stress-related
mechanisms
underlying
progress
In
addition,
correlated
with
provide
potential
therapeutic
targets
develop
safe
effective
treatments
Here,
we
summarized
main
strategies
control
this
disease.
Annual Review of Immunology,
Journal Year:
2020,
Volume and Issue:
38(1), P. 567 - 595
Published: Feb. 4, 2020
Caspases
are
a
family
of
conserved
cysteine
proteases
that
play
key
roles
in
programmed
cell
death
and
inflammation.
In
multicellular
organisms,
caspases
activated
via
macromolecular
signaling
complexes
bring
inactive
procaspases
together
promote
their
proximity-induced
autoactivation
proteolytic
processing.
Activation
ultimately
results
execution
death,
the
nature
this
is
determined
by
specific
involved.
Pioneering
new
research
has
unraveled
distinct
cross
talk
regulation
inflammation,
innate
immune
responses.
In-depth
understanding
these
mechanisms
essential
to
foster
development
precise
therapeutic
targets
treat
autoinflammatory
disorders,
infectious
diseases,
cancer.
This
review
focuses
on
governing
caspase
activation
with
special
emphasis
recent
progress
caspase-driven
gasdermin
D-induced
pyroptosis.
Cell Death Discovery,
Journal Year:
2021,
Volume and Issue:
7(1)
Published: July 26, 2021
Abstract
Ferroptosis,
a
recently
identified
and
iron-dependent
cell
death,
differs
from
other
death
such
as
apoptosis,
necroptosis,
pyroptosis,
autophagy-dependent
death.
This
form
of
does
not
exhibit
typical
morphological
biochemical
characteristics,
including
shrinkage,
mitochondrial
fragmentation,
nuclear
condensation.
The
dysfunction
lipid
peroxide
clearance,
the
presence
redox-active
iron
well
oxidation
polyunsaturated
fatty
acid
(PUFA)-containing
phospholipids
are
three
essential
features
ferroptosis.
Iron
metabolism
peroxidation
signaling
increasingly
recognized
central
mediators
Ferroptosis
plays
an
important
role
in
regulation
oxidative
stress
inflammatory
responses.
Accumulating
evidence
suggests
that
ferroptosis
is
implicated
variety
cardiovascular
diseases
atherosclerosis,
stroke,
ischemia-reperfusion
injury,
heart
failure,
indicating
targeting
will
present
novel
therapeutic
approach
against
diseases.
Here,
we
provide
overview
features,
process,
function,
mechanisms
ferroptosis,
its
connected
relevance
to
stress,
inflammation,
Frontiers in Cellular and Infection Microbiology,
Journal Year:
2019,
Volume and Issue:
9
Published: Nov. 26, 2019
Cell
death
is
central
to
development,
organismal
homeostasis,
and
immune
responses.
The
cell
field
has
experienced
tremendous
progress
by
delineating
the
molecular
programs
specific
each
of
apoptotic
inflammatory
pathways.
Moreover,
discovery
inflammasomes
pyroptosis
necroptosis
pathway
regulators
have
provided
genetic
basis
for
programmed
Earlier
research
highlighted
unique
regulation
these
pathways,
but
emerging
studies
discovered
co-regulation
crosstalk
between
seemingly
different
complexes.
in
this
area
led
an
idea
that
master
play
roles
orchestrating
multiple
Here,
we
provide
a
brief
review
regulators,
innate
sensor
ZBP1
essential
survival
kinase
TAK1,
vital
RIPK1/RIPK3-FADD-caspase-8
complex
assembly
its
versatility
executing
Pyroptosis,
Apoptosis,
Necroptosis,
which
dubbed
here
as
PAN-optosis.
Furthermore,
discuss
implications
therapeutic
potential
targeting
health
disease.ZBP1
TAK1
regulate
Frontiers in Immunology,
Journal Year:
2022,
Volume and Issue:
13
Published: Nov. 1, 2022
The
endothelium
is
a
single
layer
of
epithelium
covering
the
surface
vascular
system,
and
it
represents
physical
barrier
between
blood
vessel
wall
that
plays
an
important
role
in
maintaining
intravascular
homeostasis.
However,
endothelial
dysfunction
or
cell
death
can
cause
disruption,
vasoconstriction
diastolic
dysfunction,
smooth
muscle
proliferation
migration,
inflammatory
responses,
thrombosis,
which
are
closely
associated
with
progression
several
diseases,
such
as
atherosclerosis,
hypertension,
coronary
atherosclerotic
heart
disease,
ischemic
stroke,
acute
lung
injury,
kidney
diabetic
retinopathy,
Alzheimer’s
disease.
Oxidative
stress
caused
by
overproduction
reactive
oxygen
species
(ROS)
mechanism
underlying
death.
Growing
evidence
suggests
ROS
trigger
various
ways,
including
pyroptosis,
parthanatos,
ferroptosis.
Therefore,
this
review
will
systematically
illustrate
source
cells
(ECs);
reveal
molecular
ferroptosis
ECs;
provide
new
ideas
for
research
treatment
dysfunction-related
diseases.
Circulation Research,
Journal Year:
2020,
Volume and Issue:
127(3), P. 427 - 447
Published: July 16, 2020
Cardiac
fibrosis
is
mediated
by
the
activation
of
resident
cardiac
fibroblasts,
which
differentiate
into
myofibroblasts
in
response
to
injury
or
stress.
Although
myofibroblast
formation
a
physiological
acute
injury,
such
as
myocardial
infarction,
persistence,
occurs
heart
failure,
contributes
maladaptive
remodeling
and
progressive
functional
decline.
traditional
pathways
activation,
TGFβ
(transforming
growth
factor
β)
AngII
(angiotensin
II),
have
been
well
characterized,
less
understood
are
alterations
mitochondrial
function
cellular
metabolism
that
necessary
initiate
sustain
function.
In
this
review,
we
highlight
recent
reports
detailing
metabolic
mechanisms
contribute
differentiation,
with
hope
identifying
novel
therapeutic
targets
treat,
potentially
reverse,
tissue
organ
fibrosis.