Advanced Science,
Год журнала:
2024,
Номер
unknown
Опубликована: Окт. 3, 2024
Abstract
Disruptions
of
the
eukaryotic
plasma
membrane
due
to
chemical
and
mechanical
challenges
are
frequent
detrimental
thus
need
be
repaired
maintain
proper
cell
function
avoid
death.
However,
cellular
mechanisms
involved
in
wound
resealing
restoration
homeostasis
diverse
contended.
Here,
it
is
shown
that
clathrin‐mediated
endocytosis
induced
at
later
stages
repair
following
actual
wound.
This
compensatory
occurs
near
wound,
predominantly
sites
previous
early
endosome
exocytosis
which
required
initial
stage
resealing,
suggesting
a
spatio‐temporal
co‐ordination
exo‐
during
repair.
Using
cytoskeletal
alterations
modulations
tension
area,
identified
as
major
regulator
wounding‐associated
endocytic
events
mediate
efficient
Thus,
changes
universal
trigger
for
modulating
endosomes
subsequent
acting
restore
function.
Although
the
age
of
genome
gave
us
much
insight
about
how
our
organs
fail
with
disease,
it
also
suggested
that
diseases
do
not
arise
from
mutations
alone;
rather,
they
develop
as
we
age.
In
this
Review,
examine
wound
healing
might
act
to
ignite
disease.
Wound
works
well
when
are
younger,
repairing
damage
accidents,
environmental
assaults,
and
battles
pathogens.
Yet,
accumulation
tissue
damage,
repair
process
can
devolve,
leading
inflammation,
fibrosis,
neoplastic
signaling.
We
discuss
healthy
responses
bodies
misappropriate
these
pathways
in
focus
predominantly
on
epithelial-based
(lung
skin)
diseases,
similar
operate
cardiac,
muscle,
neuronal
diseases.
Frontiers in Cell and Developmental Biology,
Год журнала:
2025,
Номер
13
Опубликована: Фев. 21, 2025
Glioblastoma
(GBM)
is
the
most
malignant
of
astrocytomas,
primarily
involving
cerebral
hemispheres
and
cortex.
It
one
fatal
refractory
solid
tumors
with
a
5-year
survival
rate
only
5%
in
adults.
Cells
biological
tissues
are
subjected
to
mechanical
forces,
including
hydrostatic
pressure,
shear
stress,
compression
tension.
can
convert
mechanomechanical
signals
into
or
electrical
signals,
process
known
as
signaling.
Piezo1
channels,
members
Piezo
family
mechanosensitive
ion
be
directly
activated
by
stimuli
alone,
mediating
cation
currents
that
activate
subsequent
signaling
pathways.
Studies
have
shown
largely
unexpressed
normal
brain
but
expressed
at
high
levels
glioblastoma
significantly
contribute
development
progression,
its
role
pathogenesis
remains
unclear.
We
reviewed
relevant
literature
data
six
major
databases
PubMed,
EMBASE,
CINAHL,
Scopus,
Web
Science
TCGA.
Finally,
total
126
papers
were
selected
for
review
analysis
(Search
terms
include:
glioblastoma,
piezo1,
biomechanical,
targeted
therapy,
mechanomechanical,
extracellular
matrix,
radiation
therapy
more).
The
piezo1
was
summarized.
affects
several
fundamental
pathophysiological
processes
such
tissue
sclerosis,
angiogenesis,
energy
supply,
immune
cell
infiltration,
used
an
indicator
malignancy
prognosis
patients
well
therapeutic
target
control
tumor
progression.
pathological
mechanism
very
complex,
aberrant
expression
plays
important
glioblastoma.
Specific
mechanistic
studies
focusing
on
will
help
us
understand
mechanobiology
develop
new
approaches
patients.
Science Signaling,
Год журнала:
2025,
Номер
18(886)
Опубликована: Май 13, 2025
The
behavior
of
cells
is
governed
by
signals
originating
from
their
local
environment,
including
mechanical
forces
exerted
on
the
cells.
Forces
are
transduced
mechanosensitive
proteins,
which
can
impinge
signaling
cascades
that
also
activated
growth
factors.
We
investigated
cross-talk
between
and
biochemical
in
regulation
intracellular
networks
epithelial
monolayers.
Phosphoproteomic
transcriptomic
analyses
monolayers
subjected
to
strain
revealed
activation
extracellular
signal–regulated
kinase
(ERK)
downstream
epidermal
factor
receptor
(EGFR)
as
a
predominant
strain-induced
event.
Strain-induced
EGFR-ERK
depended
E-cadherin
adhesions.
Proximity
labeling
showed
metalloproteinase
ADAM17,
an
enzyme
mediates
shedding
soluble
EGFR
ligands,
was
closely
associated
with
E-cadherin.
A
probe
we
developed
monitor
ADAM-mediated
demonstrated
induced
ADAM
activation.
Mechanically
essential
for
mechanosensitive,
E-cadherin–dependent
signaling.
Together,
our
data
demonstrate
adhesion
triggers
ligands
stimulate
ERK
activity.
Our
findings
illustrate
how
operate
within
linear
cascade.
Current Opinion in Cell Biology,
Год журнала:
2023,
Номер
84, С. 102217 - 102217
Опубликована: Авг. 11, 2023
Extracellular
signal-regulated
kinase
(ERK)
has
been
recognized
as
a
critical
regulator
in
various
physiological
and
pathological
processes.
Extensive
research
elucidated
the
signaling
mechanisms
governing
ERK
activation
via
biochemical
regulations
with
upstream
molecules,
particularly
receptor
tyrosine
kinases
(RTKs).
However,
recent
advances
have
highlighted
role
of
mechanical
forces
activating
RTK–ERK
pathways,
thereby
opening
new
avenues
into
mechanochemical
interplay
multicellular
tissues.
Here,
we
review
force-induced
cells
propose
possible
mechanosensing
underlying
mechanoresponsive
activation.
We
conclude
that
are
not
merely
passive
factors
shaping
tissues
but
also
active
regulators
cellular
pathways
controlling
collective
cell
behaviors.
Cellular and Molecular Life Sciences,
Год журнала:
2023,
Номер
80(12)
Опубликована: Ноя. 10, 2023
The
coupling
between
mechanical
forces
and
modulation
of
cell
signalling
pathways
is
essential
for
tissue
plasticity
their
adaptation
to
changing
environments.
Whilst
the
number
physiological
pathological
relevant
roles
mechanotransduction
has
been
rapidly
expanding
over
last
decade,
studies
have
mostly
focussing
on
a
limited
mechanosensitive
pathways,
which
include
instance
Hippo/YAP/TAZ
pathway,
Wnt/β-catenin
or
stretch-activated
channel
Piezo.
However,
recent
development
spreading
new
live
sensors
provided
insights
into
contribution
ERK
pathway
in
mechanosensing
various
systems,
emerges
now
as
fast
modular
pathway.
In
this
review,
we
will
document
key
vivo
vitro
examples
that
established
clear
link
deformation,
stress
signalling,
comparing
timescale
stress.
We
then
discuss
different
molecular
mechanisms
proposed
so
far,
epistatic
mechanics
discussing
cellular
parameters
affecting
signalling.
finish
by
consequences
mechanics,
outlining
how
interplay
instrumental
self-organisation
long-range
cell-cell
coordination.
British Journal of Pharmacology,
Год журнала:
2024,
Номер
unknown
Опубликована: Авг. 8, 2024
Background
and
Purpose
Previous
studies
have
shown
that
Src
can
regulate
inflammation
tumour
progression.
However,
the
mechanisms
by
which
regulates
inflammatory
response
of
vascular
endothelium
atherogenesis
are
currently
poorly
understood.
This
study
aimed
to
investigate
role
in
endothelial
atherogenesis,
as
well
underlying
mechanisms.
Experimental
Approach
Real‐time
quantitative
PCR
was
used
measure
mRNA
levels
genes.
The
phosphorylation
localization
proteins
were
examined
using
western
blotting
immunofluorescence,
respectively.
level
p‐Src
Y416
mouse
directly
determined
en
face
staining.
Endothelial‐specific
knockdown
achieved
tail
vein
injection
AAV‐sgSrc
ApoE
−/−
;
Cas9
LSL/LSL
Cdh5‐cre
mice.
Atherosclerosis
induced
partial
ligation
carotid
artery.
Key
Results
Oscillatory
shear
stress
(OSS)
promotes
at
cells,
Piezo1
is
required
for
this
regulatory
process.
Overexpression
constitutively
active
inflammation,
Stat3
(at
Y705)
its
nuclear
translocation.
Endothelial
OSS
abolished
inhibitor
dasatinib
or
si‐Src.
Dasatinib,
when
administered
orally,
reduced
plaque
formation
mice
artery
ligation.
Additionally,
decreased
ligated
left
with
endothelial‐specific
knockdown.
Conclusion
Implications
Disturbed
flow
through
Piezo1‐Src‐Stat3
pathway.
Therefore,
inhibiting
cells
could
be
a
promising
therapeutic
strategy
treat
atherogenesis.
