Frontiers in Cell and Developmental Biology,
Journal Year:
2022,
Volume and Issue:
10
Published: March 7, 2022
Mitochondria
are
well
known
as
the
centre
of
energy
metabolism
in
eukaryotic
cells.
However,
they
can
not
only
generate
ATP
through
tricarboxylic
acid
cycle
and
oxidative
phosphorylation
but
also
control
mode
cell
death
various
mechanisms,
especially
regulated
(RCD),
such
apoptosis,
mitophagy,
NETosis,
pyroptosis,
necroptosis,
entosis,
parthanatos,
ferroptosis,
alkaliptosis,
autosis,
clockophagy
oxeiptosis.
These
mitochondria-associated
modes
lead
to
a
variety
diseases.
During
growth,
these
programmed,
meaning
that
be
induced
or
predicted.
Mitochondria-based
treatments
have
been
shown
effective
many
trials.
Therefore,
mitochondria
great
potential
for
treatment
In
this
review,
we
discuss
how
involved
death,
basic
research
latest
clinical
progress
related
fields.
We
detail
organ
system
diseases
mitochondria,
including
nervous
diseases,
cardiovascular
digestive
respiratory
endocrine
urinary
cancer.
highlight
role
play
suggest
possible
therapeutic
directions
pressing
issues
need
addressed
today.
Because
key
comprehensive
understanding
help
provide
more
strategies
treatment.
Endocrine Reviews,
Journal Year:
2021,
Volume and Issue:
42(6), P. 839 - 871
Published: March 8, 2021
The
endoplasmic
reticulum
(ER)
hosts
linear
polypeptides
and
fosters
natural
folding
of
proteins
through
ER-residing
chaperones
enzymes.
Failure
the
ER
to
align
compose
proper
protein
architecture
leads
accumulation
misfolded/unfolded
in
lumen,
which
disturbs
homeostasis
provoke
stress.
Presence
stress
initiates
cytoprotective
unfolded
response
(UPR)
restore
or
instigates
a
rather
maladaptive
UPR
promote
cell
death.
Although
wide
array
cellular
processes
such
as
persistent
autophagy,
dysregulated
mitophagy,
secretion
proinflammatory
cytokines
may
contribute
onset
progression
cardiometabolic
diseases,
it
is
well
perceived
that
also
evokes
development
particularly
cardiovascular
diseases
(CVDs),
diabetes
mellitus,
obesity,
chronic
kidney
disease
(CKD).
Meanwhile,
these
pathological
conditions
further
aggravate
stress,
creating
vicious
cycle.
Here
this
review,
we
aimed
at
summarizing
updating
available
information
on
CVDs,
CKD,
hoping
offer
novel
insights
for
management
comorbidities
regulation
Frontiers in Cardiovascular Medicine,
Journal Year:
2021,
Volume and Issue:
8
Published: May 5, 2021
Heart
failure
(HF)
patients
often
suffer
from
multiple
comorbidities,
such
as
diabetes,
atrial
fibrillation,
depression,
chronic
obstructive
pulmonary
disease,
and
kidney
disease.
The
coexistance
of
comorbidities
usually
leads
to
multi
morbidity
poor
prognosis.
Treatments
for
HF
with
are
still
an
unmet
clinical
need,
finding
effective
therapy
strategy
is
great
value.
can
lead
comorbidity,
in
return,
comorbidity
may
promote
the
progression
HF,
creating
a
vicious
cycle.
This
reciprocal
correlation
indicates
there
be
some
common
causes
biological
mechanisms.
Metabolism
remodeling
inflammation
play
vital
role
pathophysiological
processes
indicating
metabolism
links
between
comorbidities.
In
this
review,
we
comprehensively
discuss
major
underlying
mechanisms
therapeutic
implications
HF.
We
first
summarize
potential
Then,
give
overview
linkage
perspective
epidemiological
evidence
Moreover,
help
bioinformatics,
shared
risk
factors,
signal
pathways,
targets
Metabolic
syndrome,
aging,
deleterious
lifestyles
(sedentary
behavior,
dietary
patterns,
smoking,
etc.),
other
factors
all
associated
Impaired
mitochondrial
biogenesis,
autophagy,
insulin
resistance,
oxidative
stress,
among
both
Gene
enrichment
analysis
showed
PI3K/AKT
pathway
probably
central
morbidity.
Additionally,
drug
several
were
found
by
network
analysis.
Such
has
already
been
instrumental
repurposing
treat
comorbidity.
And
result
suggests
sodium-glucose
transporter-2
(SGLT-2)
inhibitors,
IL-1β
metformin
promising
drugs
propose
that
targeting
metabolic
inflammatory
pathways
provide
strategy.
Medicinal Research Reviews,
Journal Year:
2022,
Volume and Issue:
43(1), P. 5 - 30
Published: Aug. 17, 2022
Abstract
The
endoplasmic
reticulum
(ER)
governs
the
proper
folding
of
polypeptides
and
proteins
through
various
chaperones
enzymes
residing
within
ER
organelle.
Perturbation
in
process
ensues
when
overwhelmed
protein
exceeds
handling
capacity,
leading
to
accumulation
misfolded/unfolded
lumen—a
state
being
referred
as
stress.
In
turn,
stress
induces
a
gamut
signaling
cascades,
termed
“unfolded
response”
(UPR)
that
reinstates
homeostasis
panel
gene
expression
modulation.
This
type
UPR
is
usually
deemed
“adaptive
UPR.”
However,
persistent
or
unresolved
hyperactivates
response,
which
ultimately,
triggers
cell
death
inflammatory
pathways,
“maladaptive/terminal
A
plethora
evidence
indicates
crosstalks
between
(maladaptive
UPR)
inflammation
precipitate
obesity
pathogenesis.
this
regard,
acquisition
mechanisms
linking
might
unveil
potential
remedies
tackle
pathological
condition.
Herein,
we
aim
elucidate
key
stress‐induced
context
summarize
therapeutic
strategies
management
maneuvering
stress‐associated
inflammation.
Biomedicine & Pharmacotherapy,
Journal Year:
2023,
Volume and Issue:
159, P. 114171 - 114171
Published: Jan. 13, 2023
Mitochondrial
dysfunction
is
the
main
cause
of
damage
to
pathological
mechanism
ischemic
cardiomyopathy.
In
addition,
mitochondrial
can
also
affect
homeostasis
cardiomyocytes
or
endothelial
cell
dysfunction,
leading
a
vicious
cycle
oxidative
stress.
And
an
important
basis
for
cardiomyopathy
and
reperfusion
injury
after
myocardial
infarction
end-stage
coronary
heart
disease.
Therefore,
mitochondria
be
used
as
therapeutic
targets
against
ischemia
injury,
regulation
morphology,
function
structure
key
way
targeting
quality
control
mechanisms.
includes
mechanisms
such
mitophagy,
dynamics
(mitochondrial
fusion/fission),
biosynthesis,
unfolded
protein
responses.
Among
them,
increase
fragmentation
caused
by
fission
initial
factor.
The
protective
fusion
strengthen
interaction
synthesis
paired
promote
biosynthesis.
hypoxia,
formation
fragments,
fragmented
lead
damaged
DNA
production,
which
biosynthesis
insufficient
ATP
ROS.
Burst
growth
loss
membrane
potential.
This
eventually
leads
accumulation
mitochondria.
Then,
under
leadership
complete
degradation
process
through
transport
morphologically
structurally
lysosomes
degradation.
But
once
increases,
may
activate
pathway
cardiomyocyte
death.
Although
laboratory
studies
have
found
that
variety
mitochondrial-targeted
drugs
reduce
protect
cardiomyocytes,
there
are
still
few
successfully
passed
clinical
trials.
this
review,
we
describe
role
MQS
in
ischemia/hypoxia-induced
physiopathology
elucidate
relevant
further
explained
advantages
natural
products
improving
protecting
cells
from
perspective
pharmacological
mechanism,
its
related
Potential
targeted
therapies
improve
ischemia/hypoxia
discussed,
aiming
accelerate
development
cardioprotective
dysfunction.
Experimental & Molecular Medicine,
Journal Year:
2023,
Volume and Issue:
55(1), P. 269 - 280
Published: Jan. 19, 2023
Abstract
Mitochondrial
DNA
(mtDNA)
released
through
protein
oligomers,
such
as
voltage-dependent
anion
channel
1
(VDAC1),
triggers
innate
immune
activation
and
thus
contributes
to
liver
fibrosis.
Here,
we
investigated
the
role
of
Parkin,
an
important
regulator
mitochondria,
its
regulation
VDAC1-mediated
mtDNA
release
in
The
circulating
mitochondrial
levels
Parkin
VDAC1
were
upregulated
patients
with
A
4-week
CCl
4
challenge
induced
mtDNA,
STING
signaling,
a
decline
autophagy,
apoptosis
mouse
livers,
knockout
aggravated
these
effects.
In
addition,
reduced
prevented
oligomerization
manner
dependent
on
E3
activity
hepatocytes.
We
found
that
site-specific
ubiquitination
at
lysine
53
by
interrupted
into
cytoplasm
under
stress.
ubiquitination-defective
K53R
mutant
predominantly
formed
oligomers
resisted
suppression
Parkin.
Hepatocytes
expressing
exhibited
activated
signaling
pathway
hepatic
stellate
cells,
this
effect
could
not
be
abolished
propose
specific
site
confers
protection
against
fibrosis
interrupting
release.
