Research Square (Research Square),
Год журнала:
2023,
Номер
unknown
Опубликована: Ноя. 20, 2023
Abstract
Exposure
to
crystalline
silica
particle
leads
silicosis
characterized
as
progressive
fibrosis.
Fibroblasts
are
described
vital
effector
cells
in
fibrogenesis.
Emerging
studies
identified
immune
sentinel
role
of
fibroblasts
chronic
disease,
while
their
immune-modulatory
remained
elusive.
Herein,
we
confirmed
that
a
conversion
ILC2
ILC1
closely
involved
was
mediated
by
activated
fibroblast
via
IL-18.
Mechanistically,
Notch3
signaling
mechanics-activated
modulated
IL-18
production.
The
mice
specific
knockout
exerted
retardatory
progression
pulmonary
fibrosis
tightly
linked
attenuated
ILCs.
Our
results
indicated
the
activated-fibroblast
silicotic
lung
served
regulator
ILC2-ILC1
associated
with
Notch3-IL-18
axis.
findings
broadened
cognitive
boundaries
regulation
silicosis,
also
provide
potential
therapeutic
targets
treating
fibrotic
diseases.
Abstract
Background
Dilation
may
be
the
first
right
ventricular
change
and
accelerates
progression
of
threatening
tachyarrhythmias
heart
failure
for
patients
with
arrhythmogenic
cardiomyopathy
(ARVC),
but
treatment
dilation
remains
limited.
Methods
Single-cell
RNA
sequencing
(scRNA-seq)
blood
biventricular
myocardium
from
8
study
participants
was
performed,
including
6
end-stage
ARVC
2
normal
controls.
ScRNA-seq
data
then
deeply
analyzed,
cluster
annotation,
cellular
proportion
calculation,
characterization
developmental
trajectories
interactions.
An
integrative
analysis
our
single-cell
published
genome-wide
association
study-based
provided
insights
into
cell-specific
contributions
to
cardiac
arrhythmia
phenotype
ARVC.
Desmoglein
(Dsg2)
mut/mut
mice
were
used
as
model
verify
therapeutic
effects
pharmacological
intervention
on
identified
cluster.
Results
Right
ventricle
enriched
CCL3
+
proinflammatory
macrophages
TNMD
fibroblasts.
Fibroblasts
preferentially
affected
in
perturbations
associated
overlap
those
reside
genetic
variants
arrhythmia.
Proinflammatory
strongly
interact
fibroblast.
Pharmacological
inhibition
Nod-like
receptor
protein
3
(NLRP3),
a
transcriptional
factor
predominantly
expressed
by
several
other
myeloid
subclusters,
could
significantly
alleviate
dysfunction
Dsg2
(an
mouse
model).
Conclusions
This
comprehensive
lineage-specific
changes
at
resolution.
NLRP3
prevent
Clinical and Translational Medicine,
Год журнала:
2024,
Номер
14(1)
Опубликована: Янв. 1, 2024
Abstract
Background
The
impact
of
fibroblasts
on
the
immune
system
provides
insight
into
function
fibroblasts.
In
various
tissue
microenvironments,
multiple
fibroblast
subtypes
interact
with
immunocytes
by
secreting
growth
factors,
cytokines,
and
chemokines,
leading
to
wound
healing,
fibrosis,
escape
cancer
surveillance.
However,
specific
mechanisms
involved
in
fibroblast‐immunocyte
interaction
network
have
not
yet
been
fully
elucidated.
Main
body
conclusion
Therefore,
we
systematically
reviewed
molecular
interactions
from
history
cellular
evolution
cell
subtype
divisions
regulatory
networks
between
immunocytes.
We
also
discuss
how
these
communications
different
organ
statuses,
as
well
potential
therapies
targeting
reciprocal
interplay
fibrosis.
A
comprehensive
understanding
functional
cells
under
pathophysiological
conditions
which
they
communicate
may
lead
development
effective
Cell Reports,
Год журнала:
2024,
Номер
43(2), С. 113751 - 113751
Опубликована: Фев. 1, 2024
The
premetastatic
niche
(PMN)
contributes
to
lung-specific
metastatic
tropism
in
osteosarcoma.
However,
the
crosstalk
between
primary
tumor
cells
and
lung
stromal
is
not
clearly
defined.
Here,
we
dissect
composition
of
immune
PMN
identify
granulocytic
myeloid-derived
suppressor
cell
(gMDSC)
infiltration
as
positively
associated
with
immunosuppressive
formation
colonization.
Osteosarcoma-cell-derived
extracellular
vesicles
(EVs)
activate
interstitial
macrophages
initiate
influx
gMDSCs
via
secretion
chemokine
CXCL2.
Proteomic
profiling
EVs
reveals
that
EV-packaged
S100A11
stimulates
Janus
kinase
2/signal
transducer
activator
transcription
3
signaling
pathway
by
interacting
USP9X.
High
level
expression
or
circulating
correlates
presentation
metastasis
poor
prognosis
osteosarcoma
patients.
In
summary,
a
key
role
tumor-derived
formation,
providing
potential
strategies
for
monitoring
preventing
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(14), С. 7654 - 7654
Опубликована: Июль 12, 2024
Respiratory
dust
of
different
particle
sizes
in
the
environment
causes
diverse
health
effects
when
entering
human
body
and
makes
acute
or
chronic
damage
through
multiple
systems
organs.
However,
precise
toxic
potential
mechanisms
induced
by
have
not
been
systematically
summarized.
In
this
study,
we
described
sources
characteristics
three
dust:
PM2.5
(<2.5
μm),
silica
(<5
nanosilica
(<100
nm).
Based
on
their
respective
characteristics,
further
explored
main
toxicity
silica,
PM2.5,
vivo
vitro.
Furthermore,
evaluated
implications
respiratory
body,
especially
proposed
synergistic
effects,
considering
current
studies.
summary,
review
summarized
hazards
associated
with
sizes.
It
could
provide
new
insights
for
investigating
co-exposure
to
mixed
environments.
Deleted Journal,
Год журнала:
2025,
Номер
2(1), С. 10001 - 10001
Опубликована: Янв. 1, 2025
Idiopathic
pulmonary
fibrosis
(IPF)
is
a
progressive,
irreversible,
and
fatal
disease
with
an
increasing
incidence
limited
therapeutic
options.
It
characterized
by
the
formation
deposition
of
excess
extracellular
matrix
proteins
resulting
in
gradual
replacement
normal
lung
architecture
fibrous
tissue.
The
cellular
molecular
mechanism
IPF
has
not
been
fully
understood.
A
hallmark
fibroblast
to
myofibroblast
transformation
(FMT).
During
excessive
repair
upon
exposure
harmful
stimuli,
fibroblasts
transform
into
myofibroblasts
under
stimulation
cytokines,
chemokines,
vesicles
from
various
cells.
These
mediators
interact
fibroblasts,
initiating
multiple
signaling
cascades,
such
as
TGFβ1,
MAPK,
Wnt/β-catenin,
NF-κB,
AMPK,
endoplasmic
reticulum
stress,
autophagy,
contributing
FMT.
Furthermore,
single-cell
transcriptomic
analysis
revealed
significant
heterogeneity
among
myofibroblasts,
which
arise
cell
types
are
adapted
altered
microenvironment
during
pathological
repair.
This
review
provides
overview
recent
research
on
origins
pathways
driving
their
formation,
focus
interactions
between
epithelial
cells,
endothelial
macrophages
context
fibrosis.
Based
these
insights,
targeting
FMT
could
offer
promising
avenues
for
treatment
IPF.
