International Journal of Molecular Sciences,
Journal Year:
2021,
Volume and Issue:
22(14), P. 7369 - 7369
Published: July 9, 2021
Cancer
is
a
serious
health
problem
with
high
mortality
rate
worldwide.
Given
the
relevance
of
mitochondria
in
numerous
physiological
and
pathological
mechanisms,
such
as
adenosine
triphosphate
(ATP)
synthesis,
apoptosis,
metabolism,
cancer
progression
drug
resistance,
mitochondrial
genome
(mtDNA)
analysis
has
become
great
interest
study
human
diseases,
including
cancer.
To
date,
number
variants
mutations
have
been
identified
different
types
tumors,
which
coexist
normal
alleles,
phenomenon
named
heteroplasmy.
This
mechanism
considered
an
intermediate
state
between
fixation
or
elimination
acquired
mutations.
It
suggested
that
mutations,
confer
adaptive
advantages
to
tumor
growth
invasion,
are
enriched
malignant
cells.
Notably,
many
recent
studies
reported
heteroplasmy-shifting
potential
shaper
treatment
response,
we
suggest
each
type
also
unique
profile.
So
far,
plethora
data
evidencing
correlations
among
heteroplasmy
cancer-related
phenotypes
available,
but
still,
not
authentic
demonstrations,
whether
variation
mtDNA
copy
(mtCNV)
cause
consequence
remained
unknown.
Further
needed
support
these
findings
decipher
their
clinical
implications
impact
field
discovery
aimed
at
treating
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(3), P. 1428 - 1428
Published: Jan. 24, 2024
Telomere
shortening,
chromosomal
damage,
and
mitochondrial
dysfunction
are
major
initiators
of
cell
aging
biomarkers
many
diseases.
However,
the
underlying
correlations
between
nuclear
DNA
alterations
remain
unclear.
We
investigated
relationship
telomere
length
(TL)
micronucleus
(MN)
their
association
with
copy
number
(mtDNAcn)
in
peripheral
blood
mononuclear
cells
(PBMCs)
response
to
100
μM
200
hydrogen
peroxide
(H2O2)
at
44,
72,
96
h.
Significant
TL
shortening
was
observed
after
both
doses
H2O2
all
times
(all
p
<
0.05).
A
concomitant
increase
MN
found
72
h
(p
0.01)
persisted
0.01).
An
mtDNAcn
=
0.04)
µM
also
found.
In
PBMCs
treated
H2O2,
a
significant
inverse
correlation
(r
−0.76,
0.03),
mtDNA
content
directly
correlated
0.6,
inversely
related
−0.78,
0.02).
is
main
triggering
mechanism
damage
stimulated
T
lymphocytes
under
oxidative
stress.
The
support
notion
telomere–mitochondria
axis
that
might
influence
age-associated
pathologies
be
target
for
development
relevant
anti-aging
drugs.
Oxidative Medicine and Cellular Longevity,
Journal Year:
2021,
Volume and Issue:
2021(1)
Published: Jan. 1, 2021
The
integrity
and
function
of
mitochondria
are
essential
for
normal
kidney
physiology.
Mitochondrial
DNA
(mtDNA)
has
been
widely
a
concern
in
recent
years
because
its
abnormalities
may
result
disruption
aerobic
respiration,
cellular
dysfunction,
even
cell
death.
Particularly,
aberrant
mtDNA
copy
number
(mtDNA‐CN)
is
associated
with
the
development
acute
injury
chronic
disease,
urinary
mtDNA‐CN
shows
potential
to
be
promising
indicator
clinical
diagnosis
evaluation
function.
Several
lines
evidence
suggest
that
also
trigger
innate
immunity,
leading
inflammation
fibrosis.
In
mechanism,
can
released
into
cytoplasm
under
stress
recognized
by
multiple
DNA‐sensing
mechanisms,
including
Toll‐like
receptor
9
(TLR9),
cytosolic
cGAS‐stimulator
interferon
genes
(STING)
signaling,
inflammasome
activation,
which
then
mediate
downstream
inflammatory
cascades.
this
review,
we
summarize
characteristics
these
mtDNA‐sensing
pathways
mediating
responses
their
role
pathogenesis
injury,
nondiabetic
diabetic
disease.
addition,
highlight
targeting
mtDNA‐mediated
as
novel
therapeutic
target
diseases.
International Journal of Molecular Sciences,
Journal Year:
2021,
Volume and Issue:
22(14), P. 7369 - 7369
Published: July 9, 2021
Cancer
is
a
serious
health
problem
with
high
mortality
rate
worldwide.
Given
the
relevance
of
mitochondria
in
numerous
physiological
and
pathological
mechanisms,
such
as
adenosine
triphosphate
(ATP)
synthesis,
apoptosis,
metabolism,
cancer
progression
drug
resistance,
mitochondrial
genome
(mtDNA)
analysis
has
become
great
interest
study
human
diseases,
including
cancer.
To
date,
number
variants
mutations
have
been
identified
different
types
tumors,
which
coexist
normal
alleles,
phenomenon
named
heteroplasmy.
This
mechanism
considered
an
intermediate
state
between
fixation
or
elimination
acquired
mutations.
It
suggested
that
mutations,
confer
adaptive
advantages
to
tumor
growth
invasion,
are
enriched
malignant
cells.
Notably,
many
recent
studies
reported
heteroplasmy-shifting
potential
shaper
treatment
response,
we
suggest
each
type
also
unique
profile.
So
far,
plethora
data
evidencing
correlations
among
heteroplasmy
cancer-related
phenotypes
available,
but
still,
not
authentic
demonstrations,
whether
variation
mtDNA
copy
(mtCNV)
cause
consequence
remained
unknown.
Further
needed
support
these
findings
decipher
their
clinical
implications
impact
field
discovery
aimed
at
treating
