International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
26(1), С. 84 - 84
Опубликована: Дек. 25, 2024
Canine
distemper
(CD)
is
a
highly
infectious
disease
of
dogs
which
caused
by
canine
virus
(CDV).
Previous
studies
have
demonstrated
that
CDV
infection
can
induce
autophagy
in
cells.
However,
the
mechanism
underlying
CDV-induced
remains
not
fully
understood.
The
non-structural
protein
V
plays
vital
role
viral
replication
and
pathogenicity
host.
In
this
study,
we
investigated
relationship
between
CDV-V
induction
further
explored
its
impact
on
behind
this.
Our
results
showed
induced
via
inhibiting
phosphorylation
PI3K,
AKT,
mTOR
to
promote
replication.
activation
or
inhibition
PI3K
resulted
enhancing
reducing
replication,
respectively.
Further
revealed
interacted
with
cellular
autophagy.
present
study
PI3K/AKT
signaling
pathway
enhance
improve
understanding
molecular
offer
new
perspectives
for
development
effective
treatment
prevention
strategies.
Frontiers in Pharmacology,
Год журнала:
2024,
Номер
15
Опубликована: Авг. 5, 2024
Sepsis-induced
acute
lung
injury
(ALI)
is
a
major
cause
of
death
among
patients
with
sepsis
in
intensive
care
units.
By
analyzing
model
sepsis-induced
ALI
using
lipopolysaccharide
(LPS)
and
cecal
ligation
puncture
(CLP),
treatment
methods
strategies
to
protect
against
were
discussed,
which
could
provide
an
experimental
basis
for
the
clinical
ALI.
Recent
studies
have
found
that
imbalance
autophagy,
ferroptosis,
pyroptosis
key
mechanism
triggers
ALI,
regulating
these
mechanisms
can
improve
injuries
caused
by
LPS
or
CLP.
This
article
summarized
reviewed
regulatory
networks
their
important
roles
process
LPS/CLP-induced
sepsis,
discusses
possible
targeted
drugs
above
effects,
describes
dilemma
prospects,
provides
new
perspectives
future
Frontiers in Microbiology,
Год журнала:
2024,
Номер
15
Опубликована: Авг. 26, 2024
Sepsis
is
a
syndrome
precipitated
by
immune
dysregulation
in
response
to
infection,
and
represents
pivotal
factor
global
mortality
attributed
diseases.
The
recent
consensus
delineates
sepsis
as
perilous
state
of
organ
dysfunction
arising
from
the
host’s
maladaptive
reaction
infection.
It
masks
complexity
breadth
mechanisms
involved
sepsis,
which
characterized
simultaneous
hyperinflammation
immunosuppression.
highly
correlated
with
response,
mainly
mediated
various
cells
their
interactions.
This
can
lead
plethora
complications,
encompassing
systemic
inflammatory
metabolic
disturbances,
infectious
shock,
MODS,
DIC.
Furthermore,
more
research
studies
have
been
conducted
on
past
few
years.
pathological
characteristics
improved
or
treated
targeting
signaling
pathways
like
NF-B,
JAK–STAT,
PI3K-Akt,
p38-MAPK.
Combined
drug
therapy
better
than
single
for
sepsis.
article
will
review
latest
progress
pathogenesis
treatment
Heliyon,
Год журнала:
2024,
Номер
10(13), С. e33996 - e33996
Опубликована: Июль 1, 2024
Acute
lung
injury
(ALI)
is
a
condition
characterized
by
inflammation
and
oxidative
damage.
3-methyladenine
(3-MA)
has
great
potential
for
regulating
apoptosis,
but
its
regulatory
role
in
ALI
unknown.
Current Opinion in Hematology,
Год журнала:
2024,
Номер
unknown
Опубликована: Окт. 18, 2024
Purpose
of
review
Sepsis-induced
inflammatory
lung
injury
includes
acute
(ALI)
and
respiratory
distress
syndrome
(ARDS).
There
are
currently
no
effective
treatments
for
ALI/ARDS,
but
clinical
outcomes
could
be
improved
by
inhibiting
and/or
promoting
post-sepsis
vascular
repair.
In
this
review,
we
describe
studies
endothelial
cell
metabolic
pathways
in
sepsis-induced
ALI/ARDS
repair
identify
areas
research
that
deserve
attention
future
studies.
We
also
interventions
aim
to
inhibit
promote
repair,
including
those
target
metabolites,
signaling
pathways,
metabolism.
Recent
findings
Endothelial
cells
integral
both
the
phases
ALI/ARDS.
During
phase
survival
decreases,
cell-to-endothelial
(EC-EC)
junctions
weakened.
after
injury,
proliferation
EC-EC
junction
reannealing
occur.
These
crucial
aspects
is,
viability,
growth,
integrity,
controlled
a
myriad
metabolites
cells.
Summary
Metabolic
represent
novel
class
putative
targets
prevention
treatment
injury.
Therapies
being
explored
as
potential
Open Life Sciences,
Год журнала:
2024,
Номер
19(1)
Опубликована: Янв. 1, 2024
Sepsis-induced
acute
lung
injury
is
associated
with
epithelial
cell
injury.
This
study
analyzed
the
role
of
antimicrobial
peptide
LL37
mitochondrial
DNA
(LL37-mtDNA)
and
its
potential
mechanism
action
in
lipopolysaccharide
(LPS)-treated
rat
type
II
alveolar
cells
(RLE-6TN
cells).
RLE-6TN
were
treated
LPS
alone
or
LL37-mtDNA,
followed
by
transcriptome
sequencing.
Differentially
expressed
pivotal
genes
screened
using
bioinformatics
tools.
The
effects
LL37-mtDNA
on
viability,
inflammation,
apoptosis,
reactive
oxygen
species
(ROS)
production,
autophagy-related
hallmark
expression
evaluated
LPS-treated
cells.
Additionally,
Hsp90aa1
silencing
following
treatment
investigated
vitro.
further
suppressed
augmented
promoted
release
inflammatory
cytokines,
increased
ROS
elevated
LC3B
Using
sequencing
bioinformatics,
ten
candidate
identified,
which
three
core
verified
to
be
upregulated
+
group.
downregulation
attenuated
possibly
acted
as
a
crucial
target
counteract
autophagy
activation
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(5), С. 2545 - 2545
Опубликована: Фев. 22, 2024
Lindera
erythrocarpa,
a
flowering
plant
native
to
eastern
Asia,
has
been
reported
have
neuroprotective
activity.
However,
reports
on
the
specific
bioactive
compounds
in
L.
erythrocarpa
are
finite.
The
aim
of
this
study
was
investigate
anti-neuroinflammatory
and
effects
isolated
from
erythrocarpa.
Dihydropashanone,
compound
extract,
found
protected
mouse
hippocampus
HT22
cells
glutamate-induced
cell
death.
antioxidant
anti-inflammatory
properties
dihydropashanone
microglial
BV2
were
explored
study.
results
reveal
that
inhibits
lipopolysaccharide-induced
inflammatory
response
suppresses
activation
nuclear
factor
(NF)-κB
cells.
In
addition,
reduced
buildup
reactive
oxygen
species
induced
E2-related
2
(Nrf2)/heme
oxygenase
(HO)-1
signaling
pathway
Our
suggest
reduces
neuroinflammation
by
decreasing
NF-κB
microglia
protects
neurons
oxidative
stress
via
Nrf2/HO-1
pathway.
Thus,
our
data
offers
broad
range
applications
treatment
neurodegenerative
illnesses.