Acta Neuropathologica Communications,
Journal Year:
2020,
Volume and Issue:
8(1)
Published: April 7, 2020
Abstract
Parkinson’s
Disease
(PD)
is
a
progressive
neurodegenerative
disorder
with
no
cure.
Clinical
presentation
characterized
by
postural
instability,
resting
tremors,
and
gait
problems
that
result
from
loss
of
A9
dopaminergic
neurons
in
the
substantia
nigra
pars
compacta.
Traumatic
brain
injury
(TBI)
has
been
implicated
as
risk
factor
for
several
diseases,
but
strongest
evidence
linked
to
development
PD.
Mild
TBI
(mTBI),
most
common
defined
minimal,
if
any,
consciousness
absence
significant
observable
damage
tissue.
mTBI
responsible
56%
higher
developing
PD
U.S.
Veterans
increases
severity
injury.
While
mounting
human
studies
suggests
link
between
PD,
fundamental
questions
whether
nucleates
pathology
or
accelerates
vulnerable
populations
remains
unanswered.
Several
promising
lines
research
point
inflammation,
metabolic
dysregulation,
protein
accumulation
potential
mechanisms
through
which
can
initiate
accelerate
Amyloid
precursor
(APP),
alpha
synuclein
(α-syn),
hyper-phosphorylated
Tau,
TAR
DNA-binding
43
(TDP-43),
are
some
frequently
reported
proteins
upregulated
following
also
closely
Recently,
upregulation
Leucine
Rich
Repeat
Kinase
2
(LRRK2),
found
mice
TBI.
Subset
Rab
were
identified
biological
substrates
LRRK2,
extensively
late
onset
Inhibition
LRRK2
was
be
neuroprotective
models.
The
goal
this
review
survey
current
literature
concerning
mechanistic
overlap
particular
focus
on
aforementioned
proteins.
This
will
cover
application
rodent
models
further
our
understanding
relationship
Autophagy,
Journal Year:
2019,
Volume and Issue:
15(7), P. 1182 - 1198
Published: Feb. 11, 2019
Cell-based
therapies
represent
a
very
promising
strategy
to
repair
and
regenerate
the
injured
heart
prevent
progression
failure.
To
date,
these
have
had
limited
success
due
lack
of
survival
retention
infused
cells.
Therefore,
it
is
important
increase
our
understanding
biology
cells
utilize
this
information
enhance
their
function
in
heart.
Mitochondria
are
critical
for
progenitor
cell
survival.
Here,
we
demonstrate
importance
mitochondrial
autophagy,
or
mitophagy,
differentiation
process
adult
cardiac
(CPCs).
We
found
that
mitophagy
was
rapidly
induced
upon
initiation
CPCs.
also
mediated
by
receptors,
rather
than
PINK1-PRKN/PARKIN
pathway.
Mitophagy
BNIP3L/NIX
FUNDC1
not
involved
regulating
fate
determination,
biogenesis,
reprogramming.
Instead,
facilitated
CPCs
undergo
proper
network
reorganization
during
differentiation.
Abrogating
BNIP3L-
FUNDC1-mediated
led
sustained
fission
formation
donut-shaped
impaired
mitochondria.
It
resulted
increased
susceptibility
death
failure
survive
infarcted
Finally,
aging
associated
with
accumulation
DNA
(mtDNA)
damage
acquiring
mtDNA
mutations
selectively
disrupted
differentiation-activated
program
These
findings
as
regulator
differentiation,
well
consequences
accumulating
mutations.Abbreviations:
Baf:
bafilomycin
A1;
BCL2L13:
BCL2
like
13;
BNIP3:
interacting
protein
3;
BNIP3L:
3
like;
CPCs:
cells;
DM:
media;
DNM1L:
dynamin
1
EPCs:
endothelial
FCCP:
carbonyl
cyanide-4-(trifluoromethoxy)phenylhydrazone;
FUNDC1:
FUN14
domain
containing
1;
HSCs:
hematopoietic
stem
MAP1LC3B/LC3:
microtubule-associated
light
chain
beta;
MFN1/2:
mitofusin
1/2;
MSCs:
mesenchymal
mtDNA:
DNA;
OXPHOS:
oxidative
phosphorylation;
PPARGC1A:
PPARG
coactivator
alpha;
PHB2:
prohibitin
2;
POLG:
polymerase
gamma,
catalytic
subunit;
SQSTM1:
sequestosome
TEM:
transmission
electron
microscopy;
TMRM:
tetramethylrhodamine
methyl
ester
Histochemistry and Cell Biology,
Journal Year:
2018,
Volume and Issue:
150(5), P. 443 - 471
Published: Sept. 15, 2018
Peroxisomes
are
key
metabolic
organelles,
which
contribute
to
cellular
lipid
metabolism,
e.g.
the
β-oxidation
of
fatty
acids
and
synthesis
myelin
sheath
lipids,
as
well
redox
balance.
Peroxisomal
dysfunction
has
been
linked
severe
disorders
in
man,
but
peroxisomes
now
also
recognized
protective
organelles
with
a
wider
significance
human
health
potential
impact
on
large
number
globally
important
diseases
such
neurodegeneration,
obesity,
cancer,
age-related
disorders.
Therefore,
interest
their
physiological
functions
significantly
increased
recent
years.
In
this
review,
we
intend
highlight
discoveries,
advancements
trends
peroxisome
research,
present
an
update
continuation
two
former
review
articles
addressing
unsolved
mysteries
astonishing
organelle.
We
summarize
novel
findings
biological
peroxisomes,
biogenesis,
formation,
membrane
dynamics
division,
peroxisome–organelle
contacts
cooperation.
Furthermore,
peroxisomal
proteins
machineries
at
discussed.
Finally,
address
role
brain,
neurological
disorders,
development
cancer.
Redox Biology,
Journal Year:
2019,
Volume and Issue:
26, P. 101255 - 101255
Published: June 15, 2019
Nearly
130
years
after
the
first
insights
into
existence
of
mitochondria,
new
rolesassociated
with
these
organelles
continue
to
emerge.
As
essential
hubs
that
dictate
cell
fate,
mitochondria
integrate
physiology,
signaling
pathways
and
metabolism.
Thus,
recent
research
has
focused
on
understanding
how
multifaceted
functions
can
be
used
improve
inflammatory
responses
prevent
cellular
dysfunction.
Here,
we
describe
role
development
function
immune
cells,
highlighting
metabolic
aspects
pointing
out
some
metabolic-
independent
features
sustain
function.
Molecular Cancer,
Journal Year:
2019,
Volume and Issue:
18(1)
Published: March 30, 2019
Field
cancerization
and
metastasis
are
the
leading
causes
for
cancer
recurrence
mortality
in
patients.
The
formation
of
primary,
secondary
tumors
or
is
greatly
influenced
by
multifaceted
tumor-stroma
interactions,
which
stromal
components
tumor
microenvironment
(TME)
can
affect
behavior
cells.
Many
studies
have
identified
cytokines
growth
factors
as
cell
signaling
molecules
that
aid
to
communication.
However,
functional
contribution
reactive
oxygen
species
(ROS),
a
family
volatile
chemicals,
communication
less
understood.
Cancer
cells
various
tumor-associated
produce
secrete
copious
amount
ROS
into
TME.
Intracellular
modulate
cascades
acquisition
several
hallmarks
cancers.
Extracellular
help
propagate,
amplify,
effectively
create
mutagenic
oncogenic
field
facilitate
multifoci
act
springboard
metastatic
In
this
review,
we
summarize
our
current
knowledge
atypical
paracrine
metastasis.
often
discussed
separately;
offer
model
placed
these
events
with
focal
instigating
agent
broader
"seed-soil"
hypothesis.
Frontiers in Cell and Developmental Biology,
Journal Year:
2021,
Volume and Issue:
9
Published: Aug. 6, 2021
Reactive
oxygen
species
(ROS),
superoxide
anion
and
hydrogen
peroxide,
are
generated
as
byproducts
of
oxidative
phosphorylation
in
the
mitochondria
or
via
cell
signaling-induced
NADPH
oxidases
cytosol.
In
recent
two
decades,
a
plethora
studies
established
that
elevated
ROS
levels
by
eustress
crucial
physiological
mediators
many
cellular
developmental
processes.
this
review,
we
discuss
mechanisms
generation
regulation,
current
understanding
functions
maintenance
adult
embryonic
stem
cells,
well
process
reprogramming
to
pluripotent
state.
Recently
discovered
cell-non-autonomous
mediated
growth
factors
for
controlling
differentiation
immune
response
Drosophila
.
Importantly,
may
allow
deciphering
analogous
processes
human,
which
could
potentially
lead
development
novel
therapeutic
approaches
ROS-associated
diseases
treatment.
Circulation Research,
Journal Year:
2019,
Volume and Issue:
126(3), P. 298 - 314
Published: Dec. 10, 2019
Rationale:
Aging
is
one
of
the
strongest
risk
factors
for
atherosclerosis.
Yet
whether
aging
increases
atherosclerosis
independently
chronic
hyperlipidemia
not
known.
Objective:
To
determine
if
vascular
before
induction
enhances
atherogenesis.
Methods
and
Results:
We
analyzed
aortas
young
aged
normolipidemic
wild
type,
disease-free
mice
found
that
led
to
elevated
IL
(interleukin)-6
levels
mitochondrial
dysfunction,
associated
with
increased
mitophagy
protein
Parkin.
In
aortic
tissue
culture,
we
evidence
dysfunction
IL-6
exist
in
a
positive
feedback
loop.
triggered
acute
by
inducing
liver-specific
degradation
LDL
(low-density
lipoprotein)
receptor
combined
10-week
western
diet
atherogenesis
was
enhanced
wild-type
mice.
Hyperlipidemia
further
reduced
function
Parkin
but
Genetic
disruption
autophagy
smooth
muscle
cells
exposed
levels,
impaired
function,
Importantly,
enhancing
aged,
hyperlipidemic
via
oral
administration
spermidine
prevented
increase
Parkin,
attenuated
Conclusions:
Before
hyperlipidemia,
elevates
impairs
within
aorta,
levels.
These
age-associated
changes
prime
vasculature
exacerbate
upon
hyperlipidemia.
Our
work
implies
novel
therapeutics
aimed
at
improving
bioenergetics
or
reducing
inflammation
may
reduce
age-related
Cancer Science,
Journal Year:
2020,
Volume and Issue:
111(11), P. 4242 - 4256
Published: Sept. 21, 2020
Abstract
Abnormal
activation
of
the
nuclear
factor‐kappa
B
(NF‐κB)
signaling
pathway
is
closely
implicated
in
triple‐negative
breast
cancer
growth,
metastasis,
and
tumor
immune
escape.
In
this
study,
anti‐cancer
effects
icariin,
a
natural
flavonol
glycoside,
toward
cells
underlying
mechanisms
were
investigated.
This
investigation
showed
that
icariin
selectively
inhibited
proliferation
triggered
apoptosis
concentration‐
time‐dependent
manner,
but
exhibited
little
cytotoxicity
normal
cells.
Moreover,
induced
cell
via
mitochondria‐mediated
pathway,
as
indicated
by
upregulated
ratio
Bax/Bcl‐2
reactive
oxygen
species
induction.
Importantly,
impaired
NF‐κB/EMT
evidenced
upregulation
SIRT6,
resulting
inhibition
migration
invasion
Additionally,
oss‐128167,
an
inhibitor
dramatically
attenuated
anti‐migration
anti‐invasion
icariin.
Transcriptomic
analysis
verified
impairment
NF‐κB
led
to
selective
function
Notably,
significant
growth
anti‐pulmonary
metastasis
effect
mouse
model
MDA‐MB‐231
4T1
regulating
immunosuppressive
microenvironment.
Together,
these
results
could
effectively
trigger
inhibit
SIRT6/NF‐κB
suggesting
might
serve
potential
candidate
drug
for
treatment
cancer.
Antioxidants,
Journal Year:
2023,
Volume and Issue:
12(4), P. 782 - 782
Published: March 23, 2023
The
role
of
mitochondrial
function
in
health
and
disease
has
become
increasingly
recognized,
particularly
the
last
two
decades.
Mitochondrial
dysfunction
as
well
disruptions
cellular
bioenergetics
have
been
shown
to
be
ubiquitous
some
most
prevalent
diseases
our
society,
such
type
2
diabetes,
cardiovascular
disease,
metabolic
syndrome,
cancer,
Alzheimer’s
disease.
However,
etiology
pathogenesis
multiple
yet
elucidated,
making
it
one
significant
medical
challenges
history.
rapid
advances
knowledge
metabolism
coupled
with
novel
understanding
at
molecular
genetic
levels
show
tremendous
promise
day
elucidate
mysteries
this
ancient
organelle
order
treat
therapeutically
when
needed.
DNA
mutations,
infections,
aging,
a
lack
physical
activity
identified
major
players
diseases.
This
review
examines
complexities
function,
whose
incorporation
into
eukaryotic
cells
for
energy
purposes
was
key
survival
creation
new
species.
Among
these
complexities,
tightly
intertwined
derived
from
combustion
alimentary
substrates
oxygen
are
necessary
homeostasis,
including
production
reactive
discusses
different
etiological
mechanisms
by
which
mitochondria
could
dysregulated,
determining
fate
tissues
organs
being
protagonist
many
non–communicable
Finally,
is
canonical
evolutionary
characteristic
humans
that
remains
embedded
genes.
normalization
modern
society
led
perception
exercise
an
“intervention”.
modus
vivendi
engrained
genes
sedentary
real
intervention
collateral
effect
societies.
It
known
leads
and,
hence,
probably
becomes
factor
affecting
Since
only
stimulus
we
know
can
improve
maintain
emphasis
on
promotion
should
imperative
prevent
populations
chronic
where
involved,
individualized
prescription
crucial
“metabolic
rehabilitation”
patients.
From
lessons
learned
elite
athletes
(the
perfect
human
machines),
possible
translate
apply
concepts
betterment