Advanced Science,
Journal Year:
2020,
Volume and Issue:
7(7)
Published: Feb. 14, 2020
Abstract
Liver
fibrosis
currently
represents
a
global
health
problem
without
effective
pharmacotherapeutic
strategies.
The
clinical
translation
of
polydatin,
promising
natural
anti‐fibrotic
drug
candidate
with
broad
anti‐inflammatory
and
antioxidant
capabilities,
remains
major
challenge
due
to
its
limited
water
solubility
tissue
absorption.
Herein,
polydatin‐loaded
micelle
(PD‐MC)
based
on
reactive
oxygen
species
(ROS)
pH
dual‐sensitive
block
polymer
PEG‐P(PBEM‐
co
‐DPA)
is
developed.
exerts
great
potential
in
improving
the
biocompatibility
polydatin
shows
highly
efficient
liver‐targeted
release
response
fibrotic
microenvironment.
Both
vitro
vivo
studies
demonstrate
that
PD‐MC
can
significantly
suppress
inflammatory
oxidative
stress,
reduce
hepatocyte
apoptosis,
avert
activation
macrophages
hepatic
stellate
cells.
More
excitingly,
blank
itself
promotes
ROS
consumption
at
pathologic
site
provide
benefits.
These
favorable
therapeutic
virtues
targeting
multiple
cell
types
endow
remarkable
efficacy
minimal
side
effects
liver
treatment.
Thus,
holds
push
forward
application
approaches
against
fibrosis.
Cells,
Journal Year:
2021,
Volume and Issue:
10(5), P. 1056 - 1056
Published: April 29, 2021
Cancer
cells
alter
metabolic
processes
to
sustain
their
characteristic
uncontrolled
growth
and
proliferation.
These
alterations
include
(1)
a
shift
from
oxidative
phosphorylation
aerobic
glycolysis
support
the
increased
need
for
ATP,
(2)
glutaminolysis
NADPH
regeneration,
(3)
altered
flux
through
pentose
phosphate
pathway
tricarboxylic
acid
cycle
macromolecule
generation,
(4)
lipid
uptake,
lipogenesis,
cholesterol
synthesis,
(5)
upregulation
of
one-carbon
metabolism
production
NADH/NADPH,
nucleotides,
glutathione,
(6)
amino
metabolism,
(7)
metabolism-based
regulation
apoptosis,
(8)
utilization
alternative
substrates,
such
as
lactate
acetate.
Altered
in
cancer
is
controlled
by
tumor-host
cell
interactions,
key
oncogenes,
tumor
suppressors,
other
regulatory
molecules,
including
non-coding
RNAs.
Changes
pathways
are
dynamic,
exhibit
plasticity,
often
dependent
on
type
microenvironment,
leading
thought
Warburg
Effect
"reverse
Effect"
plasticity.
Understanding
complex
nature
these
multiple
can
development
new
therapies.
Signal Transduction and Targeted Therapy,
Journal Year:
2020,
Volume and Issue:
5(1)
Published: Oct. 7, 2020
Abstract
Nicotinamide
adenine
dinucleotide
phosphate
(NADPH)
is
an
essential
electron
donor
in
all
organisms,
and
provides
the
reducing
power
for
anabolic
reactions
redox
balance.
NADPH
homeostasis
regulated
by
varied
signaling
pathways
several
metabolic
enzymes
that
undergo
adaptive
alteration
cancer
cells.
The
reprogramming
of
renders
cells
both
highly
dependent
on
this
network
antioxidant
capacity
more
susceptible
to
oxidative
stress.
Modulating
unique
might
be
effective
strategy
eliminate
these
In
review,
we
summarize
current
existing
literatures
homeostasis,
including
its
biological
functions,
regulatory
mechanisms
corresponding
therapeutic
interventions
human
cancers,
providing
insights
into
implications
targeting
metabolism
associated
mechanism
therapy.
Cells,
Journal Year:
2019,
Volume and Issue:
8(9), P. 1055 - 1055
Published: Sept. 8, 2019
The
generation
of
reducing
equivalent
NADPH
via
glucose-6-phosphate
dehydrogenase
(G6PD)
is
critical
for
the
maintenance
redox
homeostasis
and
reductive
biosynthesis
in
cells.
also
plays
key
roles
cellular
processes
mediated
by
signaling.
Insufficient
G6PD
activity
predisposes
cells
to
growth
retardation
demise.
Severely
lacking
impairs
embryonic
development
delays
organismal
growth.
Altered
associated
with
pathophysiology,
such
as
autophagy,
insulin
resistance,
infection,
inflammation,
well
diabetes
hypertension.
Aberrant
activation
leads
enhanced
cell
proliferation
adaptation
many
types
cancers.
present
review
aims
update
existing
knowledge
concerning
emphasizes
how
modulates
signaling
affects
survival
demise,
particularly
diseases
cancer.
Exploiting
a
potential
drug
target
against
cancer
discussed.
Cells,
Journal Year:
2019,
Volume and Issue:
8(8), P. 926 - 926
Published: Aug. 18, 2019
Chemoresistance
is
a
major
problem
in
cancer
therapy
as
cells
develop
mechanisms
that
counteract
the
effect
of
chemotherapeutic
compounds,
leading
to
relapse
and
development
more
aggressive
cancers
contribute
poor
prognosis
survival
rates
treated
patients.
Cancer
stem
(CSCs)
play
key
role
this
event.
Apart
from
their
slow
proliferative
property,
CSCs
have
developed
range
cellular
processes
involve
drug
efflux,
enzymatic
inactivation
other
mechanisms.
In
addition,
microenvironment
where
evolve
(CSC
niche),
effectively
contributes
initiation,
progression
chemoresistance.
CSC
niche,
immune
cells,
mesenchymal
(MSCs),
endothelial
associated
fibroblasts
(CAFs)
maintenance
malignancy
via
secretion
factors
promote
resistance
chemotherapy.
Due
these
hinder
successful
therapies,
are
subject
intense
research
aims
at
better
understanding
behaviour
developing
efficient
targeting
therapies.
review,
we
provide
an
overview
chemoresistance,
discuss
progress
has
been
made
targeted
