Oxidative Medicine and Cellular Longevity,
Journal Year:
2021,
Volume and Issue:
2021(1)
Published: Jan. 1, 2021
The
normal
function
of
the
mitochondria
is
crucial
for
most
tissues
especially
those
that
demand
a
high
energy
supply.
Emerging
evidence
has
pointed
out
healthy
mitochondrial
closely
associated
with
heart
function.
When
these
processes
fail
to
repair
damaged
mitochondria,
cells
initiate
removal
process
referred
as
mitophagy
clear
away
defective
mitochondria.
In
cardiomyocytes,
metabolic
activity,
cell
differentiation,
apoptosis,
and
other
physiological
involved
in
major
phenotypic
alterations.
Mitophagy
alterations
may
contribute
detrimental
or
beneficial
effects
multitude
cardiac
diseases,
indicating
potential
clinical
insights
after
close
understanding
mechanisms.
Here,
we
discuss
current
opinions
progression
such
ischemic
disease,
diabetic
cardiomyopathy,
hypertrophy,
failure,
arrhythmia,
focus
on
key
molecules
related
pathways
regulation
mitophagy.
We
also
recently
reported
approaches
targeting
therapy
diseases.
Basic Research in Cardiology,
Journal Year:
2023,
Volume and Issue:
118(1)
Published: Nov. 8, 2023
Abstract
Cardiovascular
disease
(CVD)
is
a
major
threat
to
human
health,
accounting
for
46%
of
non-communicable
deaths.
Glycolysis
conserved
and
rigorous
biological
process
that
breaks
down
glucose
into
pyruvate,
its
primary
function
provide
the
body
with
energy
intermediate
products
needed
life
activities.
The
non-glycolytic
actions
enzymes
associated
glycolytic
pathway
have
long
been
found
be
development
CVD,
typically
exemplified
by
metabolic
remodeling
in
heart
failure,
which
condition
exhibits
rapid
adaptive
response
hypoxic
conditions,
occurring
early
course
failure.
It
mainly
characterized
decrease
oxidative
phosphorylation
rise
pathway,
glycolysis
considered
hallmark
remodeling.
In
addition
this,
main
source
cardiomyocytes
during
ischemia–reperfusion.
Not
only
that,
auxiliary
pathways
glycolysis,
such
as
polyol
hexosamine
pentose
phosphate
are
also
closely
related
CVD.
Therefore,
targeting
very
attractive
therapeutic
intervention
However,
relationship
between
CVD
complex,
some
preclinical
studies
confirmed
does
certain
degree
efficacy,
but
specific
role
has
yet
explored.
This
article
aims
summarize
current
knowledge
regarding
key
(including
hexokinase
(HK),
phosphoglucose
isomerase
(PGI),
phosphofructokinase-1
(PFK1),
aldolase
(Aldolase),
phosphoglycerate
metatase
(PGAM),
enolase
(ENO)
pyruvate
kinase
(PKM)
lactate
dehydrogenase
(LDH))
their
cardiovascular
diseases
(e.g.,
myocardial
infarction,
atherosclerosis)
possible
emerging
targets.
Cell Death and Disease,
Journal Year:
2024,
Volume and Issue:
15(4)
Published: April 27, 2024
Abstract
Mitochondria
are
the
centers
of
energy
and
material
metabolism,
they
also
serve
as
storage
dispatch
hubs
metal
ions.
Damage
to
mitochondrial
structure
function
can
cause
abnormal
levels
distribution
ions,
leading
cell
dysfunction
even
death.
For
a
long
time,
quality
control
pathways
such
dynamics
mitophagy
have
been
considered
inhibit
metal-induced
However,
with
discovery
new
metal-dependent
death
including
ferroptosis
cuproptosis,
increasing
evidence
shows
that
there
is
complex
relationship
between
This
article
reviews
latest
research
results
mechanisms
crosstalk
in
recent
years,
well
their
involvement
neurodegenerative
diseases,
tumors
other
order
provide
ideas
for
treatment
related
diseases.
Abstract
In
recent
years,
the
focus
on
human
inflammation
in
research
has
increased,
with
aging-related
widely
recognized
as
a
defining
characteristic
of
aging.
Inflammation
is
strongly
correlated
mitochondrial
dysfunction.
Phosphoglycerate
mutase
family
member
5
(PGAM5)
novel
modulator
homeostasis
response
to
mechanical
stimulation.
Here
we
review
structure
and
sublocalization
PGAM5,
introduce
its
importance
programmed
cell
death
summarize
crucial
roles
development
progression
inflammatory
diseases
such
pneumonia,
hepatitis,
neuroinflammation
Notably,
PGAM5
dual
effects
controlling
inflammation:
distinct
PGAM5-mediated
functions
exhibit
cellular
heterogeneity,
leading
control.
We
therefore
highlight
double-edged
sword
nature
potential
critical
regulator
innovative
therapeutic
target
inflammation.
Finally,
challenges
future
directions
use
which
properties,
molecule
clinic
are
discussed.
This
provides
insights
guide
intelligent
strategies
targeting
PGAM5-specific
regulation
treat
intractable
conditions,
well
extension
broader
application
other
achieve
more
precise
effective
treatment
outcomes.
MedComm,
Journal Year:
2025,
Volume and Issue:
6(3)
Published: Feb. 24, 2025
ABSTRACT
Programmed
cell
death,
including
necroptosis,
plays
a
critical
role
in
the
pathogenesis
of
cerebral
ischemia/reperfusion
injury
(CIRI).
Silent
information
regulator
1
(SIRT1)
has
been
identified
as
potential
therapeutic
target
for
CIRI,
yet
its
precise
regulating
necroptosis
remains
controversial.
Furthermore,
interaction
between
SIRT1
and
receptor‐interacting
protein
kinase
(RIP1)
this
context
is
not
fully
understood.
Sanpian
Decoction
(SPD),
classical
traditional
herbal
formula,
was
previously
shown
to
enhance
expression
our
studies.
Our
findings
demonstrated
that,
both
vivo
vitro,
CIRI
associated
with
decrease
levels
phosphorylated
dynamin‐related
(p‐DRP1)
at
Ser637,
alongside
an
increase
RIP1
other
necroptosis‐related
proteins.
Co‐immunoprecipitation
immunofluorescence
analyses
revealed
weakened
RIP1.
abnormal
mitochondrial
fission
dysfunction
were
mediated
through
phosphoglycerate
mutase
5–DRP1
pathway.
Notably,
SPD
treatment
improved
neurological
outcomes
reversed
these
pathological
changes
by
enhancing
SIRT1–RIP1
interaction.
In
conclusion,
study
suggests
that
promising
capable
inhibiting
mitigating
via
exhibits
activating
SIRT1,
thereby
attenuating
during
CIRI.
Oxidative Medicine and Cellular Longevity,
Journal Year:
2021,
Volume and Issue:
2021(1)
Published: Jan. 1, 2021
The
normal
function
of
the
mitochondria
is
crucial
for
most
tissues
especially
those
that
demand
a
high
energy
supply.
Emerging
evidence
has
pointed
out
healthy
mitochondrial
closely
associated
with
heart
function.
When
these
processes
fail
to
repair
damaged
mitochondria,
cells
initiate
removal
process
referred
as
mitophagy
clear
away
defective
mitochondria.
In
cardiomyocytes,
metabolic
activity,
cell
differentiation,
apoptosis,
and
other
physiological
involved
in
major
phenotypic
alterations.
Mitophagy
alterations
may
contribute
detrimental
or
beneficial
effects
multitude
cardiac
diseases,
indicating
potential
clinical
insights
after
close
understanding
mechanisms.
Here,
we
discuss
current
opinions
progression
such
ischemic
disease,
diabetic
cardiomyopathy,
hypertrophy,
failure,
arrhythmia,
focus
on
key
molecules
related
pathways
regulation
mitophagy.
We
also
recently
reported
approaches
targeting
therapy
diseases.