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Ectopic expression of telomerase safely increases health span and life span.
[werner syndrome]
The
absence
of
telomerase
from
somatic
cells
of
mammals
has
significant
consequences
for
aging
.
First
,
it
limits
the
number
of
potential
cell
divisions
and
in
so
doing
sets
limits
on
both
life
span
and
cancer
cell
proliferation
.
Second
,
shortened
telomeres
are
known
to
result
in
physiological
dysfunction
,
including
playing
a
role
in
human
diseases
such
as
Werner
syndrome
and
ataxia
telangiectasia
.
Ectopic
expression
of
the
catalytic
subunit
of
telomerase
,
telomerase
reverse
transcriptase
(
TERT
)
,
has
been
reported
to
extend
life
span
by
as
much
as
40
%
in
cancer
-resistant
mice
.
On
the
other
hand
,
ectopic
expression
of
TERT
promotes
cancer
in
normal
mice
.
However
,
transient
induction
of
TERT
by
an
astragalus-derived
compound
increases
health
span
without
an
apparent
increase
in
cancer
incidence
.
Ectopic
expression
of
TERT
using
adeno-associated
virus
serotype
9
(
AAV
9
)
-
based
gene
therapy
in
adult
mice
increases
both
health
span
and
life
span
without
increasing
cancer
incidence
.
Available
evidence
suggests
that
increases
in
life
span
may
require
both
elongated
telomeres
and
the
continuous
presence
of
telomerase
to
stimulate
the
WNT
/
β-catenin
signaling
pathway
.
The
recent
observation
that
WNT
/
β-catenin
signaling
can
stimulate
TERT
expression
raises
the
possibility
of
a
positive
feedback
loop
between
TERT
and
WNT
/
β-catenin
.
Such
a
positive
feedback
loop
implies
that
safety
must
be
carefully
considered
in
the
development
of
drugs
that
stimulate
telomerase
activity
.
Diseases
Validation
Diseases presenting
"cancer in normal mice"
symptom
werner syndrome
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