Journal of Clinical Investigation,
Journal Year:
2018,
Volume and Issue:
128(1), P. 74 - 84
Published: Jan. 1, 2018
Tissue
injury
disrupts
the
mechanical
homeostasis
that
underlies
normal
tissue
architecture
and
function.
The
failure
to
resolve
restore
gives
rise
progressive
fibrosis
is
accompanied
by
persistent
alterations
in
environment
as
a
consequence
of
pathological
matrix
deposition
stiffening.
This
Review
focuses
on
our
rapidly
growing
understanding
molecular
mechanisms
linking
altered
injury,
repair,
cellular
activation.
In
particular,
focus
which
cells
transduce
signals,
leading
transcriptional
epigenetic
responses
underlie
both
transient
cell
state
contribute
fibrosis.
Translation
these
mechanobiological
insights
may
enable
new
approaches
promote
repair
arrest
or
reverse
fibrotic
remodeling.
The Journal of Cell Biology,
Journal Year:
2016,
Volume and Issue:
215(4), P. 445 - 456
Published: Nov. 8, 2016
Cells
can
detect
and
react
to
the
biophysical
properties
of
extracellular
environment
through
integrin-based
adhesion
sites
adapt
milieu
in
a
process
called
mechanotransduction.
At
these
sites,
integrins
connect
matrix
(ECM)
with
F-actin
cytoskeleton
transduce
mechanical
forces
generated
by
actin
retrograde
flow
myosin
II
ECM
mechanosensitive
focal
proteins
that
are
collectively
termed
“molecular
clutch.”
The
transmission
across
adhesions
establishes
reciprocity
between
viscoelasticity
cellular
tension.
During
mechanotransduction,
force
allosterically
alters
functions
within
elicit
biochemical
signals
regulate
both
rapid
responses
mechanics
long-term
changes
gene
expression.
Integrin-mediated
mechanotransduction
plays
important
roles
development
tissue
homeostasis,
its
dysregulation
is
often
associated
diseases.
Science,
Journal Year:
2016,
Volume and Issue:
353(6304), P. 1157 - 1161
Published: Sept. 8, 2016
The
ability
of
cells
to
follow
gradients
extracellular
matrix
stiffness-durotaxis-has
been
implicated
in
development,
fibrosis,
and
cancer.
Here,
we
found
multicellular
clusters
that
exhibited
durotaxis
even
if
isolated
constituent
did
not.
This
emergent
mode
directed
collective
cell
migration
applied
a
variety
epithelial
types,
required
the
action
myosin
motors,
originated
from
supracellular
transmission
contractile
physical
forces.
To
explain
observed
phenomenology,
developed
generalized
clutch
model
which
local
stick-slip
dynamics
cell-matrix
adhesions
was
integrated
tissue
level
through
cell-cell
junctions.
Collective
is
far
more
efficient
than
single-cell
durotaxis;
it
thus
emerges
as
robust
mechanism
direct
during
wound
healing,
cancer
invasion.
