Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
15
Published: Nov. 13, 2024
Pyroptosis
is
a
form
of
inflammatory
programmed
cell
death,
and
activated
by
pathogen
infections
or
endogenous
danger
signals.
The
canonical
pyroptosis
process
characterized
the
inflammasome
(typically
NLRP3)-mediated
activation
caspase-1,
which
in
turn
cleaves
activates
IL-1β
IL-18,
as
well
gasdermin
D,
pore-forming
executor
protein,
leading
to
membrane
rupture,
release
proinflammatory
cytokines
damage-associated
molecular
pattern
molecules.
considered
part
innate
immune
response.
A
certain
level
can
help
eliminate
pathogenic
microorganisms,
but
excessive
lead
persistent
responses,
cause
tissue
damage.
In
recent
years,
has
emerged
crucial
contributor
development
chronic
respiratory
diseases,
such
asthma.
present
study
reviews
involvement
asthma,
terms
its
role
different
phenotypes
disease,
influence
on
various
non-immune
cells
airway.
addition,
potential
therapeutic
value
targeting
for
treatment
specific
asthma
discussed.
MedComm,
Journal Year:
2023,
Volume and Issue:
4(3)
Published: April 25, 2023
Abstract
Programmed
cell
death
(PCD)
is
regarded
as
a
pathological
form
of
with
an
intracellular
program
mediated,
which
plays
pivotal
role
in
maintaining
homeostasis
and
embryonic
development.
Pyroptosis
new
paradigm
PCD,
has
received
increasing
attention
due
to
its
close
association
immunity
disease.
inflammatory
mediated
by
gasdermin
that
promotes
the
release
proinflammatory
cytokines
contents
induced
inflammasome
activation.
Recently,
evidence
studies
shows
pyroptosis
crucial
conditions
like
cardiovascular
diseases
(CVDs),
cancer,
neurological
(NDs),
metabolic
(MDs),
suggesting
targeting
potential
intervention
for
treatment
these
diseases.
Based
on
this,
review
aims
identify
molecular
mechanisms
signaling
pathways
related
activation
summarizes
current
insights
into
complicated
relationship
between
multiple
human
(CVDs,
NDs,
MDs).
We
also
discuss
promising
novel
strategy
method
treating
focus
pathway
application
clinics.
Biomedicine & Pharmacotherapy,
Journal Year:
2024,
Volume and Issue:
174, P. 116453 - 116453
Published: March 20, 2024
Sepsis-associated
encephalopathy
(SAE),
a
common
neurological
complication
of
sepsis,
is
heterogenous
complex
clinical
syndrome
caused
by
the
dysfunctional
response
host
to
infection.
This
leads
excess
mortality
and
morbidity
worldwide.
Despite
relevance
with
high
incidence,
there
lack
understanding
for
its
both
acute/chronic
pathogenesis
therapeutic
management.
A
better
molecular
mechanisms
behind
SAE
may
provide
tools
enhance
efficacy.
Mounting
evidence
indicates
that
some
types
non-apoptotic
regulated
cell
death
(RCD),
such
as
ferroptosis,
pyroptosis,
autophagy,
contribute
SAE.
Targeting
these
RCD
meaningful
targets
future
treatments
against
review
summarizes
core
mechanism
which
We
focus
on
emerging
compounds
can
inhibit
delineate
their
beneficial
pharmacological
effects
Within
this
we
suggest
inhibition
serve
potential
strategy
Biomedicine & Pharmacotherapy,
Journal Year:
2024,
Volume and Issue:
177, P. 117085 - 117085
Published: July 6, 2024
Accumulating
evidence
strongly
support
the
key
role
of
NLRP3-mediated
pyroptosis
in
pathogenesis
and
progression
vascular
endothelial
dysfunction
associated
with
diabetes
mellitus.
Various
studies
have
demonstrated
that
activation
or
upregulation
Silent
Information
Regulation
2
homolog
(SIRT2)
exerts
inhibitory
effect
on
expression
NLRP3.
Although
1,8-cineole
has
been
found
to
protect
against
cardiovascular
diseases,
its
mechanism
diabetic
angiopathy
remain
unknown.
Therefore,
aim
this
study
was
investigate
ameliorative
through
SIRT2
human
umbilical
vein
cells
(HUVECs)
elucidate
underlying
mechanism.
The
findings
revealed
exhibited
a
protective
injury
ameliorated
pathological
alterations
thoracic
aorta
mice.
Moreover,
it
effectively
mitigated
induced
by
palmitic
acid-high
glucose
(PA-HG)
HUVECs.
Treatment
restored
reduced
levels
suppressed
elevated
pyroptosis-associated
proteins.
Additionally,
our
occurrence
NLRP3
deacetylation
physical
interaction
between
SIRT2.
inhibitor
AGK2
siRNA-SIRT2
attenuated
HUVECs
compromised
However,
overexpression
inhibited
PA-HG-induced
1,8-Cineole
regulating
SIRT2,
thereby
reducing
In
conclusion,
suggest
plays
crucial
development
angiopathy,
which
can
be
1,8-cineole.
Frontiers in Pharmacology,
Journal Year:
2025,
Volume and Issue:
16
Published: March 27, 2025
Alcoholic
liver
fibrosis
(ALF)
developed
from
long-term
excessive
alcohol
consumption,
which
causes
inflammatory
reactions,
lipid
accumulation
and
cirrhosis.
An
imbalance
in
gut
microbiota
is
a
crucial
driving
factor
for
through
the
gut-liver
axis.
This
study
aimed
to
explore
effect
of
physcion
on
ALF
associated
with
HMGB1/NLRP3
pathways
microbiota.
C57BL/6
mice
were
used
establish
animal
model
ALF,
LX-2
cells
alcohol-activated
cell
model,
intestinal
contents
collected
analyzed
by
16S
rRNA
sequencing.
Physcion
effectively
ameliorated
ALF-induced
inflammation,
collagen
deposition,
SirT1,
AMPK
phosphorylation
SREBP1
expression.
Moreover,
pyroptosis-related
proteins
(Caspase-1,
IL-1β,
GSDMD)
significantly
reduced
after
treatment.
Interestingly,
diversity
bacteria
abundance
treatment
was
higher,
while
harmful
lower
than
that
mice.
Importantly,
it
found
inhibit
both
vivo
vitro
,
suppress
extracellular
matrix
inhibiting
Collagen-I
α-SMA
finally
reverse
hepatic
stellate
activation.
Continuous
administration
HMGB1
NLRP3
inhibitors
showed
hepato-protection
model.
siRNA-mediated
knock-down
impaired
physcion-mediated
protection.
Regulation
pathway
recovered
injury
further
contributed
physcion’s
beneficial
effects.
Taken
together,
results
reveal
diminishes
inflammasome/pyroptosis
this
diminishment
hepato-protective
against
ALF.
