International Journal of Molecular Sciences,
Год журнала:
2021,
Номер
22(12), С. 6352 - 6352
Опубликована: Июнь 14, 2021
Amyotrophic
lateral
sclerosis
(ALS)
is
the
most
common
neurodegenerative
disease
of
motor
system.
It
characterized
by
degeneration
both
upper
and
lower
neurons,
which
leads
to
muscle
weakness
paralysis.
ALS
incurable
has
a
bleak
prognosis,
with
median
survival
3-5
years
after
initial
symptomatology.
In
ALS,
neurons
gradually
degenerate
die.
Many
features
mitochondrial
dysfunction
are
manifested
in
diseases,
including
ALS.
Mitochondria
have
shown
be
an
early
target
pathophysiology
contribute
progression.
Disruption
their
axonal
transport,
excessive
generation
reactive
oxygen
species,
disruption
structure,
dynamics,
mitophagy,
energy
production,
calcium
buffering
apoptotic
triggering
all
been
directly
involved
pathogenesis
extensively
reported
patients
animal
model
systems.
Alterations
production
severely
limit
capacity,
tightly
linked
redox
status
mitochondria.
The
present
review
focuses
on
this
link.
Placing
oxidative
stress
as
main
pathophysiological
mechanism,
molecular
interactions
metabolic
flows
analyzed.
This
discussing
potential
therapeutic
approaches
targeting
biology
slow
Frontiers in Endocrinology,
Год журнала:
2020,
Номер
11
Опубликована: Сен. 16, 2020
Diabetes
is
the
only
non-communicable
disease
with
pandemic
magnitude.
Essentially
defined
as
an
endocrine-metabolic
condition,
its
entangled
pathophysiology
and
broad
spectrum
of
ever
progressing
complications
has
turned
this
intense
investigational
target
that
bridges
to
cancer,
neurodegenerative
processes,
ultimately
aging.
Diabetic
environment
contains
major
stressors
for
onset
premature
cellular
senescence
precocious
organismal
Thus,
diabetic
subjects
exhibit
reduced
tissue
resilience
limited
biological
reserves
safeguarding
mechanisms
injury
counteraction.
The
impaired
wound
healing
response
illustrative
example
accounting
majority
lower
limbs
amputations
life
expectancy.
Classic
studies
seeded
notion
a
founding
pillar
orchestration
chronic
phenotype
wounds.
Tracking
diabetes
molecular
drivers
teach
glucose
derivative
glucooxidative
products
act
chain
reaction
within
progressive
vicious
circle
in
which
classic
"aging
hallmarks"
are
pathogenically
instrumental.
Mitochondrial
dysfunction
interconnected
dysmetabolism,
pro-oxidative
milieu,
inflammatory
activation
program,
conspire
against
DNA
integrity,
triggers
switches
program.
Fibroblasts,
endothelial
cells
keratinocytes
chronically
exposed
catalyze
their
These
in-wound
senescent
create
society
via
secretome
that,
paracrine
manner,
contributes
perpetuation
chronicity.
memory
turns
these
refractory
migrate,
proliferate,
secrete
granulation
ingredients
under
vivo
vitro
scenarios.
Mesenchymal
stem
also
impacted
by
diabetes-related
pro-senescence
forces,
may
translate
reduction
natural
reservoir
competent
repair,
turnover,
conservation.
Molecules,
Год журнала:
2020,
Номер
25(17), С. 3926 - 3926
Опубликована: Авг. 27, 2020
Neurodegenerative
disease
is
a
collective
term
given
for
the
clinical
condition,
which
results
in
progressive
degeneration
of
neurons
and
loss
functions
associated
with
affected
brain
region.
Apart
from
increase
age,
neurodegenerative
diseases
are
also
partly
by
diet
lifestyle
practices.
Parkinson’s
(PD)
slow
onset
disorder
second
most
common
disease,
affects
motor
system.
Although
there
no
prescribed
treatment
method
to
prevent
cure
PD,
procedures
help
manage
symptoms.
Green
tea
polyphenols
known
several
health
benefits,
including
antioxidant,
anti-inflammatory,
neuroprotective
activity.
The
current
manuscript
summarizes
possible
mechanisms
potential
green
special
focus
on
PD.
Studies
have
suggested
that
consumption
protects
against
free-radicals,
inflammation,
neuro-damages.
Several
vivo
studies
aid
understanding
overall
mechanism
tea.
However,
same
dose
may
not
be
sufficient
humans
elicit
similar
effects
due
complex
physiological,
social,
cultural
development.
Future
research
focused
more
trials
could
identify
an
optimum
impart
maximum
benefits
neuroprotection
Stem Cells,
Год журнала:
2021,
Номер
39(7), С. 913 - 928
Опубликована: Апрель 16, 2021
Abstract
Mesenchymal
stem
cells
(MSCs)
have
fueled
ample
translation
for
treatment
of
immune-mediated
diseases.
Our
previous
study
had
demonstrated
that
MSCs
could
elicit
macrophages
(Mφ)
into
anti-inflammatory
phenotypes,
and
alleviate
kidney
injury
in
diabetic
nephropathy
(DN)
mice
via
improving
mitochondrial
function
Mφ,
yet
the
specific
mechanism
was
unclear.
Recent
evidence
indicated
communicated
with
their
microenvironment
through
exchanges
mitochondria.
By
a
coculture
system
consisting
we
showed
MSCs-derived
mitochondria
(MSCs-Mito)
were
transferred
functions
improved,
which
contributed
to
M2
polarization.
Furthermore,
found
MSCs-Mito
transfer
activated
peroxisome
proliferator-activated
receptor
gamma
coactivator-1
alpha
(PGC-1α)-mediated
biogenesis.
In
addition,
PGC-1α
interacted
TFEB
high
glucose-induced
leading
elevated
lysosome-autophagy,
essential
removal
damaged
As
result,
bioenergy
capacity
combat
inflammatory
response
enhanced.
Whereas,
immune-regulatory
activity
significantly
blocked
knockdown
Mφ.
More
importantly,
be
observed
DN
mice,
adoptive
educated
Mφ
(MφMito)
inhibited
alleviated
injury.
However,
kidney-protective
effects
MφMito
abolished
when
impaired
rotenone,
similar
results
also
transfected
sipgc-1α
before
administration.
Collectively,
these
findings
suggested
elicited
phenotype
ameliorated
relied
on
PGC-1α-mediated
biogenesis
PGC-1α/TFEB-mediated
lysosome-autophagy.
International Journal of Molecular Sciences,
Год журнала:
2021,
Номер
22(12), С. 6352 - 6352
Опубликована: Июнь 14, 2021
Amyotrophic
lateral
sclerosis
(ALS)
is
the
most
common
neurodegenerative
disease
of
motor
system.
It
characterized
by
degeneration
both
upper
and
lower
neurons,
which
leads
to
muscle
weakness
paralysis.
ALS
incurable
has
a
bleak
prognosis,
with
median
survival
3-5
years
after
initial
symptomatology.
In
ALS,
neurons
gradually
degenerate
die.
Many
features
mitochondrial
dysfunction
are
manifested
in
diseases,
including
ALS.
Mitochondria
have
shown
be
an
early
target
pathophysiology
contribute
progression.
Disruption
their
axonal
transport,
excessive
generation
reactive
oxygen
species,
disruption
structure,
dynamics,
mitophagy,
energy
production,
calcium
buffering
apoptotic
triggering
all
been
directly
involved
pathogenesis
extensively
reported
patients
animal
model
systems.
Alterations
production
severely
limit
capacity,
tightly
linked
redox
status
mitochondria.
The
present
review
focuses
on
this
link.
Placing
oxidative
stress
as
main
pathophysiological
mechanism,
molecular
interactions
metabolic
flows
analyzed.
This
discussing
potential
therapeutic
approaches
targeting
biology
slow
