Cell Death Discovery,
Год журнала:
2024,
Номер
10(1)
Опубликована: Май 1, 2024
Interferon
Gamma
Inducible
Protein
16
(IFI16)
belongs
to
the
HIN-200
protein
family
and
is
pivotal
in
immunological
responses.
Serving
as
a
DNA
sensor,
IFI16
identifies
viral
aberrant
DNA,
triggering
immune
inflammatory
It
implicated
diverse
cellular
death
mechanisms,
such
pyroptosis,
apoptosis,
necroptosis.
Notably,
these
processes
are
integral
emergent
concept
of
PANoptosis,
which
encompasses
demise
pathways.
Current
research
implies
significant
regulatory
role
for
particularly
regarding
cardiac
pathologies.
This
review
delves
into
complex
interplay
between
PANoptosis
heart
diseases,
including
atherosclerosis,
myocardial
infarction,
failure,
diabetic
cardiomyopathy.
synthesizes
evidence
IFI16's
impact
on
with
intention
providing
novel
insights
therapeutic
strategies
targeting
diseases.
Journal of Biomedical Science,
Год журнала:
2023,
Номер
30(1)
Опубликована: Окт. 12, 2023
Mitochondrial
mass
and
quality
are
tightly
regulated
by
two
essential
opposing
mechanisms,
mitochondrial
biogenesis
(mitobiogenesis)
mitophagy,
in
response
to
cellular
energy
needs
other
environmental
cues.
Great
strides
have
been
made
uncover
key
regulators
of
these
complex
processes.
Emerging
evidence
has
shown
that
there
exists
a
tight
coordination
between
mitophagy
mitobiogenesis,
their
defects
may
cause
many
human
diseases.
In
this
review,
we
will
first
summarize
the
recent
advances
discovery
molecular
regulations
mitobiogenesis
then
focus
on
mechanism
signaling
pathways
involved
simultaneous
regulation
tissue
or
cultured
cells
needs,
stress,
pathophysiological
conditions.
Further
studies
crosstalk
processes
at
level
provide
better
understanding
how
cell
maintains
optimal
fitness
function
under
physiological
conditions,
which
holds
promise
for
fighting
aging
aging-related
Immunological Reviews,
Год журнала:
2023,
Номер
321(1), С. 246 - 262
Опубликована: Окт. 12, 2023
Summary
Cell
death
can
be
executed
through
distinct
subroutines.
PANoptosis
is
a
unique
inflammatory
cell
modality
involving
the
interactions
between
pyroptosis,
apoptosis,
and
necroptosis,
which
mediated
by
multifaceted
PANoptosome
complexes
assembled
via
integrating
components
from
other
modalities.
There
growing
interest
in
process
function
of
PANoptosis.
Accumulating
evidence
suggests
that
occurs
under
diverse
stimuli,
for
example,
viral
or
bacterial
infection,
cytokine
storm,
cancer.
Given
impact
across
disease
spectrum,
this
review
briefly
describes
relationships
highlights
key
molecules
formation
activation,
outlines
roles
diseases
together
with
potential
therapeutic
targeting.
We
also
discuss
important
concepts
pressing
issues
future
research.
Improved
understanding
its
mechanisms
crucial
identifying
novel
targets
strategies.
Cell Death and Disease,
Год журнала:
2023,
Номер
14(12)
Опубликована: Дек. 21, 2023
Abstract
Pyroptosis,
apoptosis,
and
necroptosis
are
mainly
programmed
cell
death
(PCD)
pathways
for
host
defense
homeostasis.
PANoptosis
is
a
newly
distinct
inflammatory
PCD
pathway
that
uniquely
regulated
by
multifaceted
PANoptosome
complexes
highlights
significant
crosstalk
coordination
among
pyroptosis
(P),
apoptosis
(A),
and/or
necroptosis(N).
Although
some
studies
have
focused
on
the
possible
role
of
PANpoptosis
in
diseases,
pathogenesis
complex
underestimated.
Furthermore,
progress
related
agonists
or
inhibitors
disorders
has
not
yet
been
thoroughly
discussed.
In
this
perspective,
we
provide
perspectives
context
diverse
pathological
conditions
human
diseases.
The
treatment
targeting
also
summarized.
conclusion,
involved
plenty
including
but
limited
to
microbial
infections,
cancers,
acute
lung
injury/acute
respiratory
distress
syndrome
(ALI/ARDS),
ischemia-reperfusion,
organic
failure.
seems
be
double-edged
sword
conditions,
as
induces
negative
impact
prognosis
like
COVID-19
ALI/ARDS,
while
provides
protection
from
HSV1
Francisella
novicida
infection,
kills
cancer
cells
suppresses
tumor
growth
colorectal
cancer,
adrenocortical
carcinoma,
other
cancers.
Compounds
endogenous
molecules
promising
therapeutic
strategies,
which
can
act
PANoptosomes-associated
members
regulate
PANoptosis.
More
researches
needed
better
understand
pathology
develop
treatment.
Cell Death and Disease,
Год журнала:
2024,
Номер
15(6)
Опубликована: Июнь 28, 2024
Abstract
S100a8/a9,
largely
released
by
polymorphonuclear
neutrophils
(PMNs),
belongs
to
the
S100
family
of
calcium-binding
proteins
and
plays
a
role
in
variety
inflammatory
diseases.
Although
S100a8/a9
has
been
reported
trigger
endothelial
cell
apoptosis,
mechanisms
S100a8/a9-induced
dysfunction
during
sepsis
require
in-depth
research.
We
demonstrate
that
high
expression
levels
suppress
Ndufa3
mitochondrial
complex
I
via
downregulation
Nrf1
expression.
Mitochondrial
deficiency
contributes
NAD
+
-dependent
Sirt1
suppression,
which
induces
disorders,
including
excessive
fission
blocked
mitophagy,
mtDNA
from
damaged
mitochondria
ultimately
activates
ZBP1-mediated
PANoptosis
cells.
Moreover,
based
on
comprehensive
scRNA-seq
bulk
RNA-seq
analyses,
S100A8/A9
hi
are
closely
associated
with
circulating
count
(a
useful
marker
damage),
S100A8
is
an
independent
risk
factor
for
poor
prognosis
patients.
Journal of Agricultural and Food Chemistry,
Год журнала:
2025,
Номер
unknown
Опубликована: Фев. 11, 2025
Mycotoxin
contamination
is
a
universal
agricultural
problem
and
critical
health
issue.
Fumonisin
B1
(FB1)
one
of
the
most
toxic
extensive
fumonisins
that
exist
in
various
agro-products
foods.
Lycopene
(LYC),
as
natural
carotenoid,
becoming
increasingly
favored
owing
to
its
oxidation
resistance.
Here,
we
aim
explore
mechanism
FB1-induced
hepatotoxicity
antagonism
LYC.
In
this
study,
our
findings
indicated
FB1
induced
mitochondrial
structure
damage
loss
function
chicken
hepatocytes.
Furthermore,
upregulated
expression
PANoptosis-related
signal
molecules.
also
reduced
levels
SIRT1
Ac-FOXO1
protein
expression,
which
then
inhibited
mitophagy.
However,
LYC
relieved
these
alterations.
Most
importantly,
knockdown
protective
effects
PANoptosis.
Our
study
provides
evidence
for
role
mycotoxin-induced
hepatocyte
injury
points
potential
target
liver
protection.
Theranostics,
Год журнала:
2024,
Номер
14(9), С. 3719 - 3738
Опубликована: Янв. 1, 2024
Autophagy
dysregulation
is
known
to
be
a
mechanism
of
doxorubicin
(DOX)-induced
cardiotoxicity
(DIC).
Mitochondrial-Endoplasmic
Reticulum
Contacts
(MERCs)
are
where
autophagy
initiates
and
autophagosomes
form.
However,
the
role
MERCs
in
DIC
remains
elusive.
FUNDC1
tethering
protein
MERCs.
We
aim
investigate
effect
DOX
on
cardiomyocytes
explore
whether
it
involved
dysregulated
DIC.
