Biomedicine & Pharmacotherapy,
Год журнала:
2023,
Номер
170, С. 115990 - 115990
Опубликована: Дек. 6, 2023
Osteoarthritis
(OA)
is
a
frequent
chronic
joint
disease
in
orthopedics
that
effects
individuals
and
society
significantly.
Obesity,
aging,
genetic
susceptibility,
misalignment
are
all
known
risk
factors
for
OA,
but
its
pathomechanism
still
poorly
understood.
Researches
have
revealed
OA
much
complex
process
related
to
inflammation,
metabolic
chondrocyte
death.
It
can
affect
parts
of
the
characterized
by
causing
death
extracellular
matrix
descent.
Previously,
was
thought
develop
from
excessive
mechanical
loading
leading
destruction
articular
cartilage.
Since
some
programmed
cell
deaths
share
pattern
destruction,
it
likely
also
involves
Even
though
apoptosis
pyroptosis
been
investigated
clarifing
solely
conventional
pathways
insufficient
understand
pathophysiology
osteoarthritis.
With
more
researches,
has
discovered
osteoarthritis
other
new
processes,
including
PANoptosis,
ferroptosis,
senescence,
strongly
associated.
Among
these,
PANoptosis
combines
key
traits
pyroptosis,
apoptosis,
necrotic
into
highly
coordinated
dynamically
balanced
inflammatory
mechanism.
Furthermore,
we
think
PANopotosis
might
obstruct
necroptosis
senescence.
Therefore,
order
offer
direction
therapeutic
treatment,
evaluate
development
research
on
multiple
chondrocytes
OA.
Pharmacological Research,
Год журнала:
2024,
Номер
200, С. 107079 - 107079
Опубликована: Янв. 24, 2024
The
AIM2
inflammasome
represents
a
multifaceted
oligomeric
protein
complex
within
the
innate
immune
system,
with
capacity
to
perceive
double-stranded
DNA
(dsDNA)
and
engage
in
diverse
physiological
reactions
disease
contexts,
including
cancer.
While
originally
conceived
as
discerning
sensor,
has
demonstrated
its
capability
discern
various
nucleic
acid
variations,
encompassing
RNA
DNA-RNA
hybrids.
Through
interaction
acids,
orchestrates
assembly
of
involving
multiple
proteins,
aptly
named
inflammasome,
which
facilitates
enzymatic
cleavage
proinflammatory
cytokines,
namely
pro-IL-1β
pro-IL-18.
This
process,
turn,
underpins
pivotal
biological
role.
In
this
review,
we
provide
systematic
summary
discussion
latest
advancements
sensing
types
acids.
Additionally,
discuss
modulation
activation,
can
cause
cell
death,
pyroptosis,
apoptosis,
autophagic
death.
Finally,
fully
illustrate
evidence
for
dual
role
different
cancer
types,
both
anti-tumorigenic
pro-tumorigenic
functions.
Considering
above
information,
uncover
therapeutic
promise
modulating
treatment.
European Journal of Clinical Investigation,
Год журнала:
2024,
Номер
54(9)
Опубликована: Апрель 17, 2024
Intervertebral
disc
degeneration
(IVDD)
is
a
common
chronic
orthopaedic
disease
in
orthopaedics
that
imposes
heavy
economic
burden
on
people
and
society.
Although
it
well
established
IVDD
associated
with
genetic
susceptibility,
ageing
obesity,
its
pathogenesis
remains
incompletely
understood.
Previously,
was
thought
to
occur
because
of
excessive
mechanical
loading
leading
destruction
nucleus
pulposus
cells
(NPCs),
but
studies
have
shown
much
more
complex
process
inflammation,
metabolic
factors
NPCs
death
can
involve
all
parts
the
disc,
characterized
by
causing
extracellular
matrix
(ECM)
degradation.
The
damage
pattern
like
some
programmed
cell
death,
suggesting
death.
apoptosis
pyroptosis
been
studied
IVDD,
intervertebral
still
not
be
fully
elucidated
using
only
traditional
modalities.
With
increasing
research,
new
modes
PANoptosis,
ferroptosis
senescence
found
closely
related
degeneration.
Among
these,
PANoptosis
combines
essential
elements
pyroptosis,
necroptosis
form
highly
coordinated
dynamically
balanced
inflammatory
process.
Furthermore,
we
believe
may
also
crosstalk
senescence.
Therefore,
review
progress
research
multiple
deaths
provide
guidance
for
clinical
treatment.
The
innate
immune
system
serves
as
the
first
line
of
host
defense.
Transforming
growth
factor-β-activated
kinase
1
(TAK1)
is
a
key
regulator
immunity,
cell
survival,
and
cellular
homeostasis.
Because
its
importance
in
several
pathogens
have
evolved
to
carry
TAK1
inhibitors.
In
response,
hosts
sense
inhibition
induce
robust
lytic
death,
PANoptosis,
mediated
by
RIPK1-PANoptosome.
PANoptosis
unique
inflammatory
death
pathway
initiated
an
sensor
driven
caspases
RIPKs.
While
can
be
beneficial
clear
pathogens,
excess
activation
linked
pathology.
Therefore,
understanding
molecular
mechanisms
regulating
inhibitor
(TAK1i)-induced
central
our
RIPK1
health
disease.
Immunological Reviews,
Год журнала:
2025,
Номер
329(1)
Опубликована: Янв. 1, 2025
ABSTRACT
Inflammasomes
are
crucial
mediators
of
both
antimicrobial
host
defense
and
inflammatory
pathology,
requiring
stringent
regulation
at
multiple
levels.
This
review
explores
the
pivotal
role
mitogen‐activated
protein
kinase
(MAPK)
signaling
in
modulating
inflammasome
activation
through
various
regulatory
mechanisms.
We
detail
recent
advances
understanding
MAPK‐mediated
NLRP3
priming,
licensing
activation,
with
emphasis
on
MAPK‐induced
activator
protein‐1
(AP‐1)
ERK1
JNK
licensing,
TAK1
connecting
death
receptor
to
activation.
Furthermore,
we
discuss
novel
insights
into
MAPK
human
NLRP1
focusing
MAP3K
member
ZAKα
as
a
key
linking
ribosomal
stress
Lastly,
work
elucidating
how
Bacillus
anthracis
lethal
toxin
(LeTx)
manipulates
induce
macrophage
apoptosis
an
immune
evasion
strategy,
counteraction
this
effect
genotype‐specific
Nlrp1b
certain
rodent
strains.
The Journal of Immunology,
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 18, 2025
Abstract
Inflammasomes
are
multiprotein
innate
immune
complexes
formed
in
response
to
infections,
tissue
damage,
or
cellular
stress
that
promote
the
maturation
and
release
of
IL-1β/IL-18
implicated
lytic
cell
death.
The
NLRP3
inflammasome
is
canonically
activated
by
an
initial
priming
event
followed
activation
stimulus,
leading
rapid
death
occurs
through
caspase-1
(CASP1)
gasdermin
D
(GSDMD)
activation,
called
pyroptosis.
CASP1-
GSDMD-deficient
cells
protected
from
LPS
plus
ATP-induced
However,
responses
physiologically
occur
over
time,
extending
beyond
minutes
hours
days.
Therefore,
this
study,
we
assessed
early
timepoints.
While
lacking
sensor
were
induced
canonical
trigger,
ATP
stimulation
(LPS
ATP),
for
extended
started
lyse
a
time-dependent
manner
after
2
h.
Nevertheless,
robust
IL-1β
IL-18
was
still
dependent
on
CASP1
activation.
These
data
suggested
engages
additional
immune,
pathway.
Indeed,
caspases
RIPKs
associated
with
PANoptosis
WT
cells,
deficient
machinery
times.
A
PANoptosome
complex
containing
NLRP3,
ASC,
CASP8,
RIPK3
observed
microscopy
WT,
as
well
GSDMD-deficient,
30
min
post-stimulation.
Overall,
these
findings
highlight
central
role
sensor.
Given
physiological
death,
PANoptosis,
health
disease,
our
study
emphasizes
importance
comprehensive
understanding
PANoptosomes,
their
components,
therapeutic
targets.
International Journal of Molecular Sciences,
Год журнала:
2023,
Номер
24(20), С. 15343 - 15343
Опубликована: Окт. 19, 2023
PANoptosis
is
a
newly
defined
programmed
cell
death
(PCD)
triggered
by
series
of
stimuli,
and
it
engages
three
well-learned
PCD
forms
(pyroptosis,
apoptosis,
necroptosis)
concomitantly.
Normally,
recognized
as
strategy
to
eliminate
unnecessary
cells,
inhibit
the
proliferation
invaded
pathogens
maintain
homeostasis;
however,
vigorous
can
cause
excessive
inflammation
tissue
damage.
Acute
lung
injury
(ALI)
chronic
obstructive
pulmonary
syndrome
(COPD)
exacerbation
related
several
(e.g.,
influenza
A
virus,
SARS-CoV-2)
known
PANoptosis.
An
understanding
mechanism
specific
regulators
may
help
address
pathological
systems
these
diseases.
This
review
presents
our
potential
role
in
different
Microbes and Infection,
Год журнала:
2023,
Номер
25(8), С. 105179 - 105179
Опубликована: Июль 1, 2023
TNF
and
IFN-γ
trigger
cell
damage
during
SARS
CoV-2
infection;
these
cytokines
can
induce
senescence
a
death
process
called
PANoptosis.
This
study
included
138
vaccine-naïve
COVID-19
patients,
who
were
divided
into
four
groups
(Gp)
according
to
the
plasma
level
of
(High
[
