Acta Physiologica,
Journal Year:
2024,
Volume and Issue:
240(6)
Published: April 29, 2024
Abstract
Piezo1
is
an
essential
mechanosensitive
transduction
ion
channel
in
mammals.
Its
unique
structure
makes
it
capable
of
converting
mechanical
cues
into
electrical
and
biological
signals,
modulating
(patho)physiological
processes
a
wide
variety
cells.
There
increasing
evidence
demonstrating
that
the
piezo1
plays
vital
role
renal
physiology
disease
conditions.
This
review
summarizes
current
on
properties
Piezo1,
gating
modulation,
pharmacological
characteristics,
with
special
focus
distribution
significance
kidney,
which
may
provide
insights
potential
treatment
targets
for
diseases
involving
this
channel.
BMC Genomics,
Journal Year:
2025,
Volume and Issue:
26(1)
Published: April 7, 2025
Differentiation
of
fibroblasts
into
myofibroblasts
is
necessary
for
wound
healing,
but
excessive
myofibroblast
presence
and
persistence
can
result
in
scarring.
Treatment
scarring
limited
largely
due
to
a
lack
comprehensive
understanding
how
differ
at
the
transcript
level.
The
purpose
this
study
was
characterize
transcriptional
profiles
injured
relative
normal
fibroblasts,
utilizing
from
vocal
fold
as
model.
Utilizing
bulk
RNA
sequencing
technology,
we
identified
differentially
expressed
genes
between
four
cell
lines
(cVFF),
one
line
scarred
(sVFF),
treated
with
transforming
growth
factor-beta
1
(TGF-β1),
representing
an
induced-scar
phenotype
(tVFF).
Principal
component
analysis
revealed
clustering
separate
TGF-β1;
were
more
similar
than
TGF-β1.
Enrichment
analyses
pathways
related
signaling,
receptor-ligand
activity,
regulation
functions
adhesion
ECM
binding
Although
transcriptomic
TGF-β1
relatively
dissimilar,
most
highly
co-expressed
enriched
actin
cytoskeleton
binding,
which
supports
use
represent
phenotype.
Transcriptomics
myofibroblasts,
including
those
retrieved
scar
Despite
large
differences
transcriptomics
tVFF
sVFF,
serve
useful
vitro
model
highlight
key
similarities
extracted
pathology,
well
expected
healthy
folds.
Journal of the American Heart Association,
Journal Year:
2025,
Volume and Issue:
unknown
Published: April 7, 2025
Background
Aortic
stenosis
due
to
deleterious
remodeling
of
the
aortic
valve
is
a
health
concern
since
it
can
be
corrected
only
by
replacement
poor
knowledge
cellular
mechanisms
involved.
Fibroblastic
valvular
interstitial
cells
(VICs)
play
central
role
in
leaflet
stiffness
trans‐differentiation
into
osteoblast‐like
leading
calcification.
The
TRPM4
(transient
receptor
potential
melastatin
4)
cation
channel
was
shown
participate
cardiac
fibroblast
remodeling.
It
also
involved
radiation‐induced
vivo
mice.
We
hypothesized
that
might
human
VIC
transition
osteoblastic
phenotype.
Methods
Human
valves
were
collected
from
patients
undergoing
surgical
replacement.
Isolated
VICs
maintained
14
days
culture
standard
or
pro‐calcifying
media
and
submitted
inhibitor
9‐phenanthrol,
small
hairpin
RNA–TRPM4.
Osteogenic
differentiation
evaluated
measuring
hydroxyapatite
crystals
Alizarin
red
staining
protein
expression
osteogenic
markers.
Results
Western
blot
on
revealed
functionality
confirmed
patch‐clamp
recordings
exhibiting
cationic
current
sensitive
voltage
internal
Ca
2+
.
exhibited
higher
mineralization
than
media,
with
an
increase
Mineralization
markers
(bone
morphogenetic
2,
runt‐related
transcription
factor
2)
decreased
when
contained
9‐phenanthrol
Similarly,
SMAD1/5
nuclear
activated
T‐cell
pathways
stimulated
conditions
compared
but
reduced
Conclusions
participates
thus
appears
as
target
prevent
View,
Journal Year:
2025,
Volume and Issue:
unknown
Published: April 17, 2025
Abstract
Myocardial
remodeling
is
a
crucial
pathophysiological
factor
underlying
heart
failure,
the
leading
cause
of
death
globally.
In
this
study,
we
utilized
confocal
Raman
spectroscopy
imaging
to
gain
unprecedented
insights
into
myocardial
tissue
during
remodeling.
We
induced
in
rats
via
subcutaneous
administration
isoproterenol
(ISO)
(5
mg/kg)
over
seven
days,
meticulously
validated
by
echocardiography
and
histopathological
staining.
Subsequent
analyses
using
transmission
electron
microscopy
revealed
significant
mitochondrial
damage.
Confocal
imaging,
however,
provided
most
detailed
visualization
complex
architecture
within
remodeled
tissue.
Notably,
technique
enabled
precise
differentiation
between
hypertrophic
fibrotic
regions
myocardium.
These
findings
not
only
deepen
our
understanding
mechanisms
driving
but
also
highlight
transformative
potential
as
label‐free,
high‐resolution
tool
for
assessing
cardiac
pathology.
Additionally,
artificial
intelligence
(AI)
assisted
identification
rapid
sites
tissues
further
enhance
technology
targeted
clinical
applications,
marking
advancement
managing
failure.
Biomolecules,
Journal Year:
2023,
Volume and Issue:
13(9), P. 1382 - 1382
Published: Sept. 12, 2023
Epigenetic
mechanisms
and
cell
crosstalk
have
been
shown
to
play
important
roles
in
the
initiation
progression
of
cardiac
fibrosis.
This
review
article
aims
provide
a
thorough
overview
epigenetic
involved
fibroblast
regulation.
During
fibrosis,
regulation
encompasses
multitude
mechanisms,
including
DNA
methylation,
histone
acetylation
chromatin
remodeling.
These
regulate
phenotype
fibroblasts
extracellular
matrix
composition
by
modulating
gene
expression,
thereby
orchestrating
Moreover,
fibrosis
disrupts
normal
function
imposing
myocardial
mechanical
stress
compromising
electrical
conduction.
also
delves
into
intricate
between
cardiomyocytes
non-cardiomyocytes
heart.
A
comprehensive
understanding
governing
is
critical
for
development
effective
therapeutic
strategies.
Further
research
warranted
unravel
precise
molecular
underpinning
these
processes
identify
potential
targets.
Frontiers in Molecular Biosciences,
Journal Year:
2023,
Volume and Issue:
10
Published: Oct. 12, 2023
Fibrosis
could
happen
in
every
organ,
leading
to
organic
malfunction
and
even
organ
failure,
which
poses
a
serious
threat
global
health.
Early
treatment
of
fibrosis
has
been
reported
be
the
turning
point,
therefore,
exploring
potential
correlates
pathogenesis
how
reverse
become
pressing
issue.
As
mechanism-sensitive
cationic
calcium
channel,
Piezo1
turns
on
response
changes
lipid
bilayer
plasma
membrane.
exerts
multiple
biological
roles,
including
inhibition
inflammation,
cytoskeletal
stabilization,
epithelial-mesenchymal
transition,
stromal
stiffness,
immune
cell
mechanotransduction,
interestingly
enough.
These
processes
are
closely
associated
with
development
fibrotic
diseases.
Recent
studies
have
shown
that
deletion
or
knockdown
attenuates
onset
fibrosis.
Therefore,
this
paper
we
comprehensively
describe
biology
gene,
focusing
its
relevance
pulmonary
fibrosis,
renal
pancreatic
cardiac
diseases,
except
for
role
drugs
(agonists),
increased
intracellular
mechanical
stress
using
gene
alleviating
Journal of Cardiothoracic Surgery,
Journal Year:
2024,
Volume and Issue:
19(1)
Published: April 15, 2024
Abstract
Background
Cardiac
fibroblasts
(CFs)
are
activated
after
initial
injury,
and
then
differentiate
into
myofibroblasts
(MFs),
which
play
a
pivotal
role
as
the
primary
mediator
cells
in
pathological
remodeling.
Sodium
butyrate
(NaB),
being
metabolite
of
gut
microbiota,
exhibits
anti-inflammatory
property
local
therapies
on
sites
other
than
intestine.
Thus,
this
study
aimed
to
probe
mechanism
by
NaB
regulates
CFs
transdifferentiation
through
NLRP3/Caspase-1
pyroptosis
pathway.
Methods
were
cultured
vitro
induced
MFs
TGFβ1.
identified
immunofluorescence
labelling
technique
vimentin
α-SMA,
followed
treatment
with
or
NLRP3
inflammasome
inhibitor
(CY-09)
its
activator
[nigericin
sodium
salt
(NSS)].
The
expression
levels
GSDMD-N/NLRP3/cleaved
Caspase-1
proteins,
inflammatory
factors
IL-1β/IL-18/IL-6/IL-10
determined
using
immunofluorescence,
Western
blot
ELISA.
Cell
proliferation
migration
evaluated
CCK-8
assay
cell
scratch
test,
respectively.
Results
Following
induction
TGFβ1,
exhibited
increased
α-SMA
proteins
IL-6/IL-10,
well
proliferative
migratory
abilities.
TGFβ1
MFs,
while
inhibited
differentiation.
inactivated
CY-09
demonstrated
inhibitory
effects
pathway,
leading
reduction
TGFβ1-induced
transdifferentiation.
NSS
thus
partially
counteracting
effect
intestinal
microbiota
Conclusion
NaB,
activation
pathway
CFs,
repressed
MFs.