Life,
Год журнала:
2024,
Номер
14(12), С. 1688 - 1688
Опубликована: Дек. 20, 2024
Aquaporins
(AQPs)
are
membrane
proteins
facilitating
water
and
other
small
solutes
to
be
transported
across
cell
membranes.
They
crucial
in
maintaining
cellular
homeostasis
by
regulating
permeability
various
tissues.
Moreover,
they
regulate
migration,
signaling
pathways,
inflammation,
tumor
growth,
metastasis.
In
critically
ill
patients,
such
as
trauma,
sepsis,
patients
with
acute
respiratory
distress
syndrome
(ARDS),
which
frequently
encountered
intensive
care
units
(ICUs),
transport
regulation
is
for
homeostasis,
dysregulation
can
lead
edema
or
dehydration,
the
latter
also
implicating
hemodynamic
compromise.
Indeed,
AQPs
involved
fluid
organs,
including
lungs,
kidneys,
brain,
where
their
dysfunction
exacerbate
conditions
like
ARDS,
kidney
injury
(AKI),
cerebral
edema.
this
review,
we
discuss
implication
of
clinical
entities
ICUs,
systemic
inflammation
AKI,
brain
due
different
types
primary
from
a
perspective.
Current
possible
future
therapeutic
implications
considered.
Journal of Advanced Research,
Год журнала:
2024,
Номер
62, С. 229 - 243
Опубликована: Март 27, 2024
Overwhelming
neutrophil
activation
and
oxidative
stress
significantly
contribute
to
acute
respiratory
distress
syndrome
(ARDS)
pathogenesis.
However,
the
potential
of
repurposing
ribociclib,
a
cyclin-dependent
kinase
4
6
(CDK4/6)
inhibitor
used
clinically
in
cancer
treatment,
for
treating
neutrophilic
ARDS
remains
uncertain.
This
study
illustrated
ability
underlying
mechanism
ribociclib
inflammation.
BMC Infectious Diseases,
Год журнала:
2025,
Номер
25(1)
Опубликована: Март 7, 2025
The
onset
of
sepsis
frequently
coincides
with
acute
respiratory
distress
syndrome
(ARDS),
which
constitutes
a
significant
contributor
to
severe
acid–base
disturbances
in
septic
patients.
In
the
pathogenesis
sepsis,
it
conducts
crucial
role.
lysosomal
metabolic
disorders
and
immune
imbalance
conduct
pivotal
Despite
extensive
research
into
alterations
status
during
few
studies
have
been
reported
thoroughly
examine
association
between
lysosomes
sepsis.
As
result,
this
study
is
predominantly
Intended
delve
link
lysosome-related
genes
lysosome
microenvironment
from
standpoint
bioinformatics
Registration
Number
was
ChiCTR1900021261.
Date
2019/02/04.
Method
Sepsis
data
source:
collected
previous
clinical
sequencing
results
(Originated
BGI
Shenzhen
Co.,
Ltd.)
GO
database
utilized
for
collection
genes.
Differential
expression
(DEGs)
were
screened
on
by
employing
IDEP
0.93
software
subsequent
quality
control.
Afterwards,
enrichment
analysis
conducted
adopting
Gene
Set
Enrichment
Analysis
(GSEA)
Weighted
Co
Network
(WGCNA),
followed
cross
referencing
identify
DEGs
associated
lysosomes.
KEGG
pathway
wereperformed
subsequently.
obtained
PLSGs
WGCNA
Creating
PPI
network
entails
following
steps:
points
intersected
at
first.
CytoHubba
MCODE
performed
utilizing
cytoscape
software.
Next,
intersection
taken
confirm
Hub
gene
sequences,
subsequently
central
tightly
existing
CTD
scores.
Notwithstanding
fact
that
causes
are
multifaceted,
ARDS
can
often
trigger
development
numerous
cases.
Simultaneously,
an
aim
predict
transcription
factor
levels
nervous
system,
Cytoscape
adopted
find
relevant
target
miRNAs
miRWalk
database,
correlated
regulatory
established
accordingly.
SEPSIS
infiltration
model
constructed
ImmuCellAI
abundance
Spearman's
method.
Last
but
not
least,
worth
noting
single-cell
has
validated
as
method
analyze
hub
cells
patients,
enabling
selection
key
closely
predictive
outcomes.
Result
When
(ARDS)
present,
differentially
expressed
implicated
metabolism
regulation
microenvironment.
Six
bound
up
or
attributable
examinations.
On
top
that,
determined
patients
had
syndrome.
illustrated
remarkable
augment
T
cell
while
relative
DC
reduced
certain
level.
Positive
correlations
found
two
Spearman
role
cells.
Moreover,
universally
acknowledged
anti-inflammatory
responsible
negative
correlation.
basis
sequencing,
CTSO
HLA-DQA1
Aside
survival-death
curve
direction
suggested
they
could
be
core
predicting
sepsis-related
prognosis
analysis.
Conclusion
An
demonstrates
interaction
changes
understanding
basis,
we
develop
new
diagnostics
therapeutic
approaches
identifying
drug
targets.
Nonetheless,
differ
simply
difference
site
infection;
etiology
cases
quite
complex,
progression
occur
if
infection
exacerbates
other
complications
arise,
meeting
diagnostic
criteria
3.0.
Pharmacognosy Magazine,
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 14, 2025
Background
Pneumonia
is
a
serious
respiratory
illness
that
impacts
the
lungs,
leading
to
inflammation
and
fluid
accumulation
in
alveoli,
tiny
air
sacs
essential
for
gas
exchange.
Mycoplasma
pneumonia
severe
infection
caused
by
atypical
bacterium
pneumoniae
(MP).
Purpose
The
primary
objective
of
this
work
explore
therapeutic
effects
ferulic
acid
against
MP-infected
an
experimental
mice
model.
Methods
In
work,
BALB/c
were
subjected
100
µL
MP
challenge
via
nasal
drips
trigger
pneumonia.
then
administered
50
mg/kg
3
days.
After
experimentation,
lung
weight,
myeloperoxidase
(MPO),
nitric
oxide
(NO)
concentrations
assessed.
inflammatory
cytokines
oxidative
stress
biomarkers
analyzed
using
appropriate
diagnostic
kits.
total
cell
count
bronchoalveolar
lavage
(BAL)
deoxyribonucleic
(DNA)
concentration
lungs
assessed
mice.
histopathology
examination
was
conducted
evaluate
histological
abnormalities.
Results
administration
significantly
decreased
MPO,
NO
Ferulic
treatment
resulted
diminution
malondialdehyde
(MDA)
enhancement
glutathione
(GSH)
superoxide
dismutase
(SOD)
concentrations.
diminished
marker
MP-challenged
Furthermore,
reduced
DNA
content
counts
addition,
outcomes
indicated
significant
reduction
alveolar
damage
with
Conclusion
findings
confirm
salutary
properties
Consequently,
may
serve
as
effective
drug
candidate
treatment.
Toxics,
Год журнала:
2025,
Номер
13(5), С. 365 - 365
Опубликована: Апрель 30, 2025
(1)
Background:
Silicosis,
a
chronic
lung
fibrosis
disorder
triggered
by
the
accumulation
of
silica
dust
in
deep
regions,
is
characterized
intricate
molecular
mechanisms.
Among
these,
NOX2
(NADPH
oxidase
2)
and
JNK
(C-Jun
N-terminal
kinase)
signaling
pathways
play
pivotal
roles
progression
pulmonary
fibrosis.
Despite
their
significance,
precise
mechanisms
underlying
crosstalk
between
these
remain
largely
unexplored.
(2)
Methods:
To
unravel
interactions,
we
examined
interplay
human
epithelial
cells
subjected
to
exposure
through
vivo
assays,
followed
validation
using
single-cell
sequencing.
Our
findings
consistently
revealed
elevated
expression
levels
key
components
from
both
pathway
lungs
silicosis-induced
mice
silica-treated
cells.
(3)
Results:
Notably,
activation
was
linked
increased
ROS
(reactive
oxygen
species)
production,
profibrogenic
factors,
diminished
cell
proliferation
silica-exposed
Further
mechanistic
analyses
demonstrated
that
amplifies
production
induced
exposure,
while
treatment
with
inhibitor
SP600125
mitigates
effects.
Conversely,
overexpression
enhanced
silica-induced
epithelial–mesenchymal
transition
(EMT)-related
whereas
knockdown
exerted
opposite
effect.
These
results
suggest
positive
feedback
loop
signaling,
which
may
drive
EMT
following
exposure.
(4)
Conclusions:
This
reciprocal
interaction
appears
critical
role
damage
pathogenesis
silicosis,
shedding
light
on
disease
offering
potential
avenues
for
therapeutic
intervention.
International Journal of Molecular Sciences,
Год журнала:
2023,
Номер
24(2), С. 1641 - 1641
Опубликована: Янв. 13, 2023
Acute
lung
injury
is
a
complex
cascade
process
that
develops
in
response
to
various
damaging
factors,
which
can
lead
acute
respiratory
distress
syndrome.
Within
this
study,
based
on
bioinformatics
reanalysis
of
available
full-transcriptome
data
induced
mice
and
humans
by
we
selected
set
genes
could
serve
as
good
targets
for
suppressing
inflammation
the
tissue,
evaluated
their
expression
cells
different
origins
during
LPS-induced
inflammation,
chose
tissue
inhibitor
metalloproteinase
Timp1
promising
target
inflammation.
We
designed
an
effective
chemically
modified
anti-TIMP1
siRNA
showed
silencing
correlates
with
decrease
pro-inflammatory
cytokine
IL6
secretion
cultured
macrophage
reduces
severity
mouse
model.
Journal of Advanced Research,
Год журнала:
2024,
Номер
unknown
Опубликована: Июль 1, 2024
Neutrophilic
inflammation,
characterized
by
dysregulated
neutrophil
activation,
triggers
a
variety
of
inflammatory
responses
such
as
chemotactic
infiltration,
oxidative
bursts,
degranulation,
extracellular
traps
(NETs)
formation,
and
delayed
turnover.
This
type
inflammation
is
pivotal
in
the
pathogenesis
acute
respiratory
distress
syndrome
(ARDS)
psoriasis.
Despite
current
treatments,
managing
neutrophil-associated
symptoms
remains
significant
challenge.
review
emphasizes
role
cyclin-dependent
kinases
(CDKs)
activation
inflammation.
It
aims
to
highlight
therapeutic
potential
repurposing
CDK
inhibitors
manage
neutrophilic
particularly
ARDS
Additionally,
it
discusses
necessary
precautions
for
clinical
application
these
due
off-target
effects
need
dose
optimization.
CDKs
regulate
key
functions,
including
responses,
NET
apoptosis.
Repurposing
inhibitors,
originally
developed
cancer
treatment,
shows
promise
controlling
Clinical
anticancer
drugs,
palbociclib
ribociclib,
have
demonstrated
efficacy
treating
psoriasis
targeting
off-label
pathways,
phosphoinositide
3-kinase
(PI3K)
phosphodiesterase
4
(PDE4),
respectively.
While
offer
promising
benefits,
their
requires
careful
consideration
Further
exploration
trials
are
ensure
safety
conditions.