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Telomere shortening in human diseases.
[werner syndrome]
The
discovery
of
telomeres
dates
back
to
the
early
20
th
century
.
In
humans
,
telomeres
are
heterochromatic
structures
with
tandem
DNA
repeats
of
5
'
-
TTAGGG-
3
'
at
the
chromosomal
ends
.
Telomere
length
varies
greatly
among
species
and
ranges
from
10
to
15
kb
in
humans
.
With
each
cell
division
,
telomeres
shorten
progressively
because
of
the
'
end-replication
problem
'
.
Short
or
dysfunctional
telomeres
are
often
recognized
as
DNA
DSBs
,
triggering
cell-cycle
arrest
and
result
in
cellular
senescence
or
apoptotic
cell
death
.
Therefore
,
telomere
shortening
serves
as
an
important
tumor
-suppressive
mechanism
by
limiting
cellular
proliferative
capacity
by
regulating
senescence
checkpoint
activation
.
Although
telomeres
serve
as
a
mitotic
clock
to
cells
,
they
also
confer
capping
on
chromosomes
,
with
help
from
telomere-associated
proteins
.
Over
the
past
decades
,
many
studies
of
telomere
biology
have
demonstrated
that
telomeres
and
telomere-associated
proteins
are
implicated
in
human
genetic
diseases
.
In
addition
,
it
has
become
more
apparent
that
accelerated
telomere
erosion
is
associated
with
a
myriad
of
metabolic
and
inflammatory
diseases
.
Moreover
,
critically
short
or
unprotected
telomeres
are
likely
to
form
telomeric
fusions
,
leading
to
genomic
instability
,
the
cornerstone
for
carcinogenesis
.
In
light
of
these
,
this
minireview
summarizes
studies
on
telomeres
and
telomere-associated
proteins
in
human
diseases
.
Elucidating
the
roles
of
telomeres
involved
in
the
mechanisms
underlying
pathogenesis
of
these
diseases
may
open
up
new
possibilities
for
novel
molecular
targets
as
well
as
provide
important
diagnostic
and
therapeutic
implications
.
Diseases
Validation
Diseases presenting
"cellular proliferative capacity"
symptom
werner syndrome
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