Cells
capable
of
cardiomyocyte-like
differentiation
have
been
in
the
limelight
for
several
years.
Such
cells
investigated
extensively
their
potential
to
regenerate
injured
heart
when
transplanted.
The
heart's
capacity
repair
is
limited,
although
some
degree
cardiomyocyte
regeneration
has
shown
occur
throughout
adulthood.
However,
elusive
nature
adult
cardiac
stem
led
inconclusive
evidence
presence.
Direct
replacement
and
delivery
electrically
active,
contractile
are
presented
with
further
challenges
related
electrical
coupling
arrhythmias.
Furthermore,
cell
types
or
progenitor
characteristics
require
extensive
manipulation,
enrichment,
expansion
before
use
as
therapy.
As
tissue
a
finely
orchestrated
interplay
types,
it
not
surprising
that
combining
endothelial
mesenchymal
promise
over
therapy
using
single
type.
An
alternative
mechanism
direct
cardiomyocytes
lost
to,
example
ischemic
damage,
stimulation
myocardium's
inherent
protective
capacities
pathways
functional
repair.
This
achievable
by
means,
including
drugs,
biomaterials,
released
soluble
factors.
In
these
approaches,
lie
targeted
long-term
efficacy
therapies.
A
recent
advance
utilization
an
individual's
autologous,
processed
micrografts
derived
from
atrial
appendages.
appendages
pouch-shaped
annexes
atria.
For
example,
left
appendage
can
contribute
formation
blood
clots,
especially
during
fibrillation,
which
rationale
its
clinical
closure
even
excision
cases.
Hence,
attractive
strategy
obtain
safely
directly
patient.
Micrograft
transplants
produced
comprehensively
harbor
most
myocardial
intricately
meshed
supporting
extracellular
matrix.
microtissue
produce
paracrine
factors,
such
natriuretic
peptides,
which,
therapeutic
viewpoint,
elucidated
convey
both
antifibrotic
cardioprotective
effects
on
myocardium.
Their
upon
open
surgery
epicardial
transplantation,
they
apt
targets
gene
applications.
chapter
provides
insight
into
current
state
autologous
micrograft
therapy,
proposed
mechanisms
action,
means
processing
transplantation
surgery.
BMC Biology,
Journal Year:
2025,
Volume and Issue:
23(1)
Published: April 30, 2025
In
adult
mammals,
including
humans,
neurons,
and
axons
in
the
brain
spinal
cord
are
inherently
incapable
of
regenerating
after
injury.
Studies
animals
with
innate
capacity
for
regeneration
providing
valuable
insights
into
mechanisms
driving
tissue
healing.
The
aim
this
review
is
to
summarize
recent
data
on
zebrafish
neonatal
mice.
We
infer
that
elucidating
these
understanding
how
why
they
lost
mammals
will
contribute
development
strategies
promote
central
nervous
system
regeneration.
Nature Communications,
Journal Year:
2025,
Volume and Issue:
16(1)
Published: April 20, 2025
Tendon
injuries
are
frequently
occurring
disorders;
it
is
clinically
important
to
enhance
tendon
regeneration
and
prevent
functional
impairment
post-injury.
While
in
children
heal
quickly
with
minimal
scarring,
those
adults
slowly
accompanied
by
fibrotic
scarring.
Therefore,
investigating
the
healing
mechanisms
after
injury,
identifying
factors
that
regulate
inherent
regenerative
capacity
of
tendons
promising
approaches
promoting
regeneration.
Here,
we
identify
PI3K-Akt
signalling
pathway
preferentially
upregulated
injured
neonatal
murine
Achilles
tendons.
Inhibition
a
rupture
model
decreases
cell
proliferation
migration
both
Scx-lineage
intrinsic
tenocytes
Tppp3-lineage
extrinsic
paratenon
sheath
cells.
Moreover,
inhibition
stemness
promotes
mature
tenogenic
differentiation
Scx-
Collectively,
these
results
suggest
plays
pivotal
role
Communications Biology,
Journal Year:
2023,
Volume and Issue:
6(1)
Published: Nov. 9, 2023
Abstract
The
potential
for
basic
research
to
uncover
the
inner
workings
of
regenerative
processes
and
produce
meaningful
medical
therapies
has
inspired
scientists,
clinicians,
patients
hundreds
years.
Decades
studies
using
a
handful
highly
model
organisms
have
significantly
advanced
our
knowledge
key
cell
types
molecular
pathways
involved
in
regeneration.
However,
many
questions
remain
about
how
unfold
regeneration-competent
species,
they
are
curtailed
non-regenerative
organisms,
might
be
induced
(or
restored)
humans.
Recent
technological
advances
genomics,
biology,
computer
science,
bioengineering,
stem
hold
promise
collectively
provide
new
experimental
evidence
different
accomplish
process
In
theory,
this
should
inform
design
clinical
approaches
medicine.
A
deeper
understanding
tissues
organs
regenerate
will
also
undoubtedly
impact
adjacent
scientific
fields.
To
best
apply
adapt
these
technologies
ways
that
break
long-standing
barriers
answer
critical
regeneration,
we
must
combine
deep
developmental
evolutionary
biologists
with
hard-earned
expertise
scientists
mechanistic
technical
end,
perspective
is
based
on
conversations
from
workshop
organized
at
Banbury
Center,
during
which
diverse
cross-section
regeneration
community
experts
various
discussed
enduring
biology.
Here,
share
group
identified
as
significant
unanswered,
i.e.,
known
unknowns.
We
describe
obstacles
limiting
progress
answering
expanding
number
diversity
used
essential
deepening
capacity.
Finally,
propose
investigating
problems
collaboratively
across
network
researchers
advance
field
unexpected
insights
into
important
related
areas
biology
Journal of Visualized Experiments,
Journal Year:
2024,
Volume and Issue:
206
Published: April 12, 2024
Resolutive
cures
for
spinal
cord
injuries
(SCIs)
are
still
lacking,
due
to
the
complex
pathophysiology.
One
of
most
promising
regenerative
approaches
is
based
on
stem
cell
transplantation
replace
lost
tissue
and
promote
functional
recovery.
This
approach
should
be
further
explored
better
in
vitro
ex
vivo
safety
efficacy
before
proceeding
with
more
expensive
time-consuming
animal
testing.
In
this
work,
we
show
establishment
a
long-term
platform
mouse
(SC)
organotypic
slices
transplanted
human
neural
cells
test
cellular
replacement
therapies
SCIs.
Standard
SC
cultures
maintained
around
2
or
3
weeks
vitro.
Here,
describe
an
optimized
protocol
maintenance
(≥30
days)
up
90
days.
The
medium
used
culturing
was
also
transplanting
into
model.
Human
SC-derived
neuroepithelial
(h-SC-NES)
carrying
green
fluorescent
protein
(GFP)
reporter
were
slices.
Thirty
days
after
transplant,
GFP
expression
low
apoptotic
rate,
suggesting
that
environment
sustained
their
survival
integration
inside
tissue.
represents
robust
reference
efficiently
testing
will
allow
researchers
perform
pre-screening
different
therapies,
helping
them
choose
appropriate
strategy
experiments.
Resolutive
cures
for
spinal
cord
injuries
(SCIs)
are
still
lacking,
due
to
the
complex
pathophysiology.
One
of
most
promising
regenerative
approaches
is
based
on
stem
cell
transplantation
replace
lost
tissue
and
promote
functional
recovery.
This
approach
should
be
further
explored
better
in
vitro
ex
vivo
safety
efficacy
before
proceeding
with
more
expensive
time-consuming
animal
testing.
In
this
work,
we
show
establishment
a
long-term
platform
mouse
(SC)
organotypic
slices
transplanted
human
neural
cells
test
cellular
replacement
therapies
SCIs.
Standard
SC
cultures
maintained
around
2
or
3
weeks
vitro.
Here,
describe
an
optimized
protocol
maintenance
(≥30
days)
up
90
days.
The
medium
used
culturing
was
also
transplanting
into
model.
Human
SC-derived
neuroepithelial
(h-SC-NES)
carrying
green
fluorescent
protein
(GFP)
reporter
were
slices.
Thirty
days
after
transplant,
GFP
expression
low
apoptotic
rate,
suggesting
that
environment
sustained
their
survival
integration
inside
tissue.
represents
robust
reference
efficiently
testing
will
allow
researchers
perform
pre-screening
different
therapies,
helping
them
choose
appropriate
strategy
experiments.
Research Square (Research Square),
Journal Year:
2024,
Volume and Issue:
unknown
Published: Oct. 23, 2024
Abstract
Effective
axon
regeneration
is
essential
for
the
successful
recovery
of
nerve
functions
in
patients
with
injury-associated
neurological
diseases.
Certain
self-regeneration
occurs
injured
peripheral
axonal
branches
dorsal
root
ganglion
(DRG)
neurons
but
does
not
occur
their
central
branches.
By
performing
rat
sciatic
or
axotomy,
we
determined
expression
dysbindin
domain
containing
2
(DBNDD2)
DRGs
after
regenerative
injury
non-regenerative
injury,
respectively,
and
found
that
DBNDD2
down-regulated
up-regulated
injury.
Moreover,
differs
neonatal
adult
gradually
increased
during
development.
knockdown
promotes
outgrowth
neurites
both
DRG
stimulates
robust
rats
crush
Bioinformatic
analysis
data
showed
transcription
factor
estrogen
receptor
1
(ESR1)
interacts
DBNDD2,
exhibits
a
similar
trend
as
may
targets
DBDNN2.
These
studies
indicate
reduced
level
low
abundance
neonates
contribute
to
thus
suggest
manipulation
promising
therapeutic
approach
improving
damage.