Biomedicine & Pharmacotherapy,
Год журнала:
2023,
Номер
167, С. 115493 - 115493
Опубликована: Сен. 19, 2023
Sepsis,
a
life-threatening
dysregulated
status
of
the
host
response
to
infection,
can
cause
multiorgan
dysfunction
and
mortality.
Sepsis
places
heavy
burden
on
cardiovascular
system
due
pathological
imbalance
hyperinflammation
immune
suppression.
Myocardial
injury
cardiac
caused
by
aberrant
responses
pathogens
lead
cardiomyopathy,
one
most
critical
complications
sepsis.
However,
many
questions
about
specific
mechanisms
characteristics
this
complication
remain
be
answered.
The
causes
sepsis-induced
include
abnormal
perfusion,
myocardial
inhibitory
substances,
autonomic
dysfunction,
mitochondrial
calcium
homeostasis
dysregulation.
fight
between
acts
as
trigger
for
cardiomyopathy.
Pyroptosis,
form
programmed
cell
death,
plays
role
in
progress
Toll-like
receptors
(TLRs)
act
pattern
recognition
participate
innate
pathways
that
recognize
damage-associated
molecular
patterns
well
pathogen-associated
mediate
pyroptosis.
Notably,
pyroptosis
is
tightly
associated
with
sepsis
septic
shock.
In
line
these
observations,
induction
TLR-mediated
may
promising
therapeutic
approach
treat
This
review
focuses
potential
roles
shed
light
approach,
thus
helping
prevent
control
shock
disorders
improve
prognosis
patients.
Biomolecules,
Год журнала:
2024,
Номер
14(3), С. 291 - 291
Опубликована: Фев. 29, 2024
Irisin,
a
novel
adipo-myokine
with
metabolic
regulatory
functions,
exerts
anti-inflammatory,
antioxidant,
and
anti-apoptotic
actions
that
may
confer
protection
against
sepsis-induced
organ
injury
in
experimental
studies.
Until
now,
only
one
human
study
has
explored
circulating
irisin
at
sepsis
onset.
We
aimed
to
examine
serum
its
kinetics
critically
ill
patients
septic
shock
regard
severity
outcome.
enrolled
102
or
within
48
h
of
diagnosis
age-
gender-matched
healthy
controls.
Irisin
was
determined
upon
enrollment
all
participants
week
later
using
an
immunoenzymatic
method.
The
outcome
recorded
28
days
after
enrollment.
At
enrollment,
significantly
lower
than
controls
(22.3
±
6.8
μg/L
vs.
28.1
6.7
μg/L,
p
<
0.001),
increased
26.6
9.5
0.001).
who
presented
those
sepsis,
non-survivors
survivors
both
later.
However,
did
not
differ
between
the
groups
(p
>
0.05).
Patients
higher
during
first
had
better
Lower
independently
associated
28-day
mortality
(sepsis
onset:
HR
0.44,
95%
C.I.
0.26–0.77,
=
0.004
after:
0.37,
0.23–0.58,
negatively
correlated
scores,
metabolic,
inflammatory
biomarkers.
Circulating
decreases
early
is
independent
predictor
mortality.
be
promising
diagnostic
prognostic
biomarker;
nevertheless,
larger
studies
are
needed
explore
role
sepsis.
PLoS ONE,
Год журнала:
2023,
Номер
18(9), С. e0291022 - e0291022
Опубликована: Сен. 1, 2023
Recently,
myocardial
ischemia-reperfusion
(I/R)
injury
was
suggested
associated
with
intestinal
flora.
However,
irisin
has
demonstrated
beneficial
effects
on
I/R
injury,
thus
increasing
interest
in
exploring
its
mechanism.
Therefore,
whether
interferes
gut
microbiota
and
mucosal
barrier
during
investigated
the
present
study.
Irisin
found
to
reduce
infiltration
of
inflammatory
cells
fracture
tissue,
enzyme
levels,
infarction
(MI)
area.
In
addition,
data
showed
that
reverses
I/R-induced
dysbiosis
as
indicated
by
decreased
abundance
Actinobacteriota
increased
Firmicutes,
maintains
integrity,
reduces
metabolic
endotoxemia,
inhibits
production
proinflammatory
cytokines
interleukin
1β
(IL-1β),
6
(IL-6),
tumor
necrosis
factor
α
(TNF-α).
Based
results,
could
be
a
good
candidate
for
ameliorating
diseases
alleviating
dysbiosis,
endothelial
dysfunction
anti-inflammatory
properties.
Journal of Inflammation Research,
Год журнала:
2024,
Номер
Volume 17, С. 5293 - 5309
Опубликована: Авг. 1, 2024
Patients
with
sepsis
frequently
develop
septic
cardiomyopathy,
which
is
known
to
be
closely
related
excessive
inflammatory
responses.
Indole-3-propionic
acid
(IPA)
a
tryptophan
metabolite
anti-inflammatory
properties
that
have
been
demonstrated
in
various
studies.
In
this
study,
we
investigated
the
underlying
mechanisms
and
therapeutic
role
of
IPA
cardiomyopathy.
British Journal of Pharmacology,
Год журнала:
2025,
Номер
unknown
Опубликована: Март 31, 2025
Abstract
Background
and
Purpose
Myocardial
dysfunction
is
a
significant
complication
associated
with
sepsis.
However,
there
are
currently
no
specific
effective
treatments
available.
Inhibiting
gasdermin
D
(GSDMD)‐mediated
pyroptosis
has
shown
promise
in
mitigating
sepsis‐induced
myocardial
dysfunction.
The
GSDMD
inhibitor
Y2
(GI‐Y2)
been
demonstrated
to
directly
bind
GSDMD.
Nonetheless,
it
remains
uncertain
whether
GI‐Y2
offers
cardioprotective
effect
the
context
of
Experimental
Approach
A
mouse
model
sepsis
was
created
using
lipopolysaccharide
(LPS),
caecal
ligation
puncture.
Following
treatment
or
macrophage
membrane‐encapsulated
nanoparticles
(GI‐Y2@MM‐NPs),
levels
heart
tissues
were
assessed.
Transcriptome
sequencing
revealed
molecular
mechanism
treating
septic
cardiomyopathy.
Key
Results
We
observed
that
alleviated
attenuated
cardiac
inflammation
mice
induced
by
LPS,
reduced
macrophage‐mediated
cardiomyocyte
injury
LPS/nigericin.
Concurrently,
we
confirmed
protective
against
LPS‐induced
abolished
absence
Additionally,
mitochondrial
damage
LPS
inhibiting
mitochondria.
Furthermore,
developed
GI‐Y2@MM‐NPs
enhance
targeting
capability
towards
macrophages
its
vivo
.
Conclusion
Implications
These
findings
indicate
alleviates
specifically
GSDMD,
thereby
GSDMD‐mediated
damage.
Both
may
serve
as
promising
therapeutic
options
for
addressing
