International Journal of Molecular Sciences,
Journal Year:
2021,
Volume and Issue:
22(16), P. 8990 - 8990
Published: Aug. 20, 2021
Altered
mitochondrial
function
is
currently
recognized
as
an
important
factor
in
atherosclerosis
initiation
and
progression.
Mitochondrial
dysfunction
can
be
caused
by
DNA
(mtDNA)
mutations,
which
inherited
or
spontaneously
acquired
various
organs
tissues,
having
more
less
profound
effects
depending
on
the
tissue
energy
status.
Arterial
wall
cells
are
among
most
vulnerable
to
due
their
barrier
metabolic
functions.
In
atherosclerosis,
mitochondria
cause
alteration
of
cellular
metabolism
respiration
known
produce
excessive
amounts
reactive
oxygen
species
(ROS)
resulting
oxidative
stress.
These
processes
involved
vascular
disease
chronic
inflammation
associated
with
atherosclerosis.
Currently,
list
mtDNA
mutations
human
pathologies
growing,
many
identified
variants
being
tested
markers.
Alleviation
stress
appears
promising
for
treatment.
this
review,
we
discuss
role
development,
focusing
key
cell
types
arterial
pathological
processes.
Accumulation
isolated
cells,
such
endothelial
may
contribute
development
local
inflammatory
process
that
helps
explaining
focal
distribution
atherosclerotic
plaques
surface.
We
also
antioxidant
anti-inflammatory
approaches
potentially
reduce
impact
dysfunction.
Theranostics,
Journal Year:
2023,
Volume and Issue:
13(2), P. 736 - 766
Published: Jan. 1, 2023
Cellular
mitophagy
means
that
cells
selectively
wrap
and
degrade
damaged
mitochondria
through
an
autophagy
mechanism,
thus
maintaining
intracellular
homeostasis.In
recent
years,
has
received
increasing
attention
as
a
research
hotspot
related
to
the
pathogenesis
of
clinical
diseases,
such
neurodegenerative
cardiovascular
cancer,
metabolic
so
on.It
been
found
regulation
may
become
new
direction
for
treatment
some
diseases.In
addition,
numerous
small
molecule
modulators
have
also
reported,
which
provides
opportunities
comprehend
procedure
potential
therapeutic
development.Taken
together,
in
this
review,
we
summarize
current
understanding
mechanism
mitophagy,
discuss
roles
its
relationship
with
introduce
existing
small-molecule
pharmacological
further
highlight
significance
their
development.
Cells,
Journal Year:
2019,
Volume and Issue:
8(7), P. 674 - 674
Published: July 3, 2019
Autophagy
(self-eating)
is
a
conserved
cellular
degradation
process
that
plays
important
roles
in
maintaining
homeostasis
and
preventing
nutritional,
metabolic,
infection-mediated
stresses.
dysfunction
can
have
various
pathological
consequences,
including
tumor
progression,
pathogen
hyper-virulence,
neurodegeneration.
This
review
describes
the
mechanisms
of
autophagy
its
associations
with
other
cell
death
mechanisms,
apoptosis,
necrosis,
necroptosis,
autosis.
has
both
positive
negative
infection,
cancer,
neural
development,
metabolism,
cardiovascular
health,
immunity,
iron
homeostasis.
Genetic
defects
such
as
static
childhood
encephalopathy
neurodegeneration
adulthood,
Crohn’s
disease,
hereditary
spastic
paraparesis,
Danon
X-linked
myopathy
excessive
autophagy,
sporadic
inclusion
body
myositis.
Further
studies
on
different
microbial
infections
could
help
to
design
develop
novel
therapeutic
strategies
against
pathogenic
microbes.
progress
prospects
research
activators
suppressors,
which
be
used
intervention
numerous
diseases
drugs
protect
human
animal
health.
Signal Transduction and Targeted Therapy,
Journal Year:
2023,
Volume and Issue:
8(1)
Published: Aug. 16, 2023
Abstract
Mitochondria
are
dynamic
organelles
with
multiple
functions.
They
participate
in
necrotic
cell
death
and
programmed
apoptotic,
crucial
for
metabolism
survival.
Mitophagy
serves
as
a
cytoprotective
mechanism
to
remove
superfluous
or
dysfunctional
mitochondria
maintain
mitochondrial
fine-tuning
numbers
balance
intracellular
homeostasis.
Growing
evidences
show
that
mitophagy,
an
acute
tissue
stress
response,
plays
important
role
maintaining
the
health
of
network.
Since
timely
removal
abnormal
is
essential
survival,
cells
have
evolved
variety
mitophagy
pathways
ensure
can
be
activated
time
under
various
environments.
A
better
understanding
diseases
treatment
therapeutic
target
design.
In
this
review,
we
summarize
molecular
mechanisms
mitophagy-mediated
elimination,
how
maintains
homeostasis
at
system
levels
organ,
what
alterations
related
development
diseases,
including
neurological,
cardiovascular,
pulmonary,
hepatic,
renal
disease,
etc.,
recent
advances.
Finally,
potential
clinical
applications
outline
conditions
regulators
enter
trials.
Research
advances
signaling
transduction
will
developing
new
strategies
precision
medicine.
Frontiers in Cardiovascular Medicine,
Journal Year:
2021,
Volume and Issue:
8
Published: Sept. 6, 2021
Atherosclerosis
is
a
chronic
lipid-driven
and
maladaptive
inflammatory
disease
of
arterial
intima.
It
characterized
by
the
dysfunction
lipid
homeostasis
signaling
pathways
that
control
inflammation.
This
article
reviews
role
inflammation
accumulation,
especially
low-density
lipoprotein
(LDL),
in
pathogenesis
atherosclerosis,
with
more
emphasis
on
cellular
mechanisms.
Furthermore,
this
review
will
briefly
highlight
medicinal
plants,
long
non-coding
RNA
(lncRNA),
microRNAs
pathophysiology,
treatment,
prevention
atherosclerosis.
Lipid
at
various
levels,
including
receptor-mediated
uptake,
synthesis,
storage,
metabolism,
efflux,
its
impairments
are
important
for
development
The
major
source
cholesterol
accumulation
wall
proatherogenic
modified
(mLDL).
Modified
lipoproteins,
such
as
oxidized
(ox-LDL)
LDL
binding
proteoglycans
extracellular
matrix
intima
blood
vessels,
cause
aggregation
particles,
endothelial
damage,
leukocyte
recruitment,
foam
cell
formation,
Inflammation
key
contributor
to
atherosclerosis
participates
all
phases
Also,
several
studies
have
shown
lncRNAs
appeared
regulators
physiological
pathophysiological
processes
regulation
HDL
biogenesis,
regulating
smooth
muscle
proliferation,
controlling
Thus,
both
immune
response
closely
linked,
their
molecular
interact
each
other.
Cellular and Molecular Immunology,
Journal Year:
2021,
Volume and Issue:
19(1), P. 67 - 78
Published: Nov. 29, 2021
The
global
coronavirus
disease
2019
(COVID-19)
pandemic
caused
by
severe
acute
respiratory
syndrome
2
(SARS-CoV-2)
has
morbidity
and
mortality
in
humans.
It
is
urgent
to
understand
the
function
of
viral
genes.
However,
open
reading
frame
10
(ORF10),
which
uniquely
expressed
SARS-CoV-2,
remains
unclear.
In
this
study,
we
showed
that
overexpression
ORF10
markedly
suppressed
expression
type
I
interferon
(IFN-I)
genes
IFN-stimulated
Then,
mitochondrial
antiviral
signaling
protein
(MAVS)
was
identified
as
target
via
suppresses
IFN-I
pathway,
MAVS
found
be
degraded
through
ORF10-induced
autophagy
pathway.
Furthermore,
promoted
accumulation
LC3
mitochondria
induced
mitophagy.
Mechanistically,
translocated
interacting
with
mitophagy
receptor
Nip3-like
X
(NIX)
its
interaction
both
NIX
LC3B.
Moreover,
knockdown
blocked
activation,
degradation,
pathway
inhibition
ORF10.
Consistent
our
observations,
context
SARS-CoV-2
infection,
inhibited
facilitated
replication.
brief,
results
reveal
a
novel
mechanism
inhibits
innate
immune
response;
is,
induces
mitophagy-mediated
degradation
binding
NIX.
Behavioral and Brain Functions,
Journal Year:
2021,
Volume and Issue:
17(1)
Published: June 12, 2021
Abstract
Aging
is
the
leading
risk
factor
for
several
age-associated
diseases
such
as
neurodegenerative
diseases.
Understanding
biology
of
aging
mechanisms
essential
to
pursuit
brain
health.
In
this
regard,
defined
by
a
gradual
decrease
in
neurophysiological
functions,
impaired
adaptive
neuroplasticity,
dysregulation
neuronal
Ca
2+
homeostasis,
neuroinflammation,
and
oxidatively
modified
molecules
organelles.
Numerous
pathways
lead
aging,
including
increased
oxidative
stress,
inflammation,
disturbances
energy
metabolism
deregulated
autophagy,
mitochondrial
dysfunction,
IGF-1,
mTOR,
ROS,
AMPK,
SIRTs,
p53
central
modulators
metabolic
control,
connecting
pathways,
which
disorders.
Also,
calorie
restriction
(CR),
physical
exercise,
mental
activities
can
extend
lifespan
increase
nervous
system
resistance
The
neuroprotective
effect
CR
involves
protection
against
ROS
generation,
maintenance
cellular
inhibition
apoptosis.
recent
evidence
about
modem
molecular
methods
neurobiology
exhibiting
significant
potential
cells
adaptation
Current Opinion in Anaesthesiology,
Journal Year:
2021,
Volume and Issue:
34(2), P. 77 - 84
Published: Feb. 4, 2021
Purpose
of
review
To
provide
a
current
overview
sepsis
pathophysiology.
Recent
findings
The
emphasis
on
pathophysiology
has
moved
away
from
the
pathogen
-
initiating
factor
and
instead
is
focussed
upon
abnormal
exaggerated
host
response.
Instead
targeted
eradication
infection,
response
activates
or
suppresses
multiple
downstream
pathways,
leading
to
organ
dysfunction.
Summary
Sepsis
represents
dysregulated
infection
Here,
triggers
an
initial
inflammatory-immune
that
leads
activation
suppression
endothelial,
hormonal,
bioenergetic,
metabolic,
immune,
other
pathways.
These,
in
turn,
produce
circulatory
metabolic
perturbations
resulting
This
will
underlying
mechanisms
propose
these
processes,
whereas
superficially
viewed
as
dysfunctional,
may
actually
be
adaptive/protective
first
instance,
though
spilling
over
into
maladaptation/harm
depending
magnitude