Oxidative Medicine and Cellular Longevity,
Journal Year:
2021,
Volume and Issue:
2021(1)
Published: Jan. 1, 2021
Fibrosis
is
the
final
common
pathology
of
most
chronic
diseases
as
seen
in
heart,
liver,
lung,
kidney,
and
skin
contributes
to
nearly
half
death
developed
countries.
Fibrosis,
or
scarring,
mainly
characterized
by
transdifferentiation
fibroblasts
into
myofibroblasts
excessive
accumulation
extracellular
matrix
(ECM)
secreted
myofibroblasts.
Despite
immense
efforts
made
field
organ
fibrosis
over
past
decades
considerable
understanding
occurrence
development
gained,
there
still
lack
an
effective
treatment
for
fibrotic
diseases.
Therefore,
identifying
a
new
therapeutic
strategy
against
unmet
clinical
need.
Naringenin,
flavonoid
that
occurs
naturally
citrus
fruits,
has
been
found
confer
wide
range
pharmacological
effects
including
antioxidant,
anti-inflammatory,
anticancer
benefits
thus
potentially
exerting
preventive
curative
on
numerous
In
addition,
emerging
evidence
revealed
naringenin
can
prevent
pathogenesis
vivo
vitro
via
regulation
various
pathways
involved
signaling
molecules
such
transforming
growth
factor-β1/small
mother
decapentaplegic
protein
3
(TGF-β1/Smad3),
mitogen-activated
kinase
(MAPK),
phosphatidylinositol
3-kinase/protein
B
(PI3K/Akt),
sirtuin1
(SIRT1),
nuclear
factor-kappa
(NF-κB),
reactive
oxygen
species
(ROS).
Targeting
these
profibrotic
could
become
novel
approach
management
disorders.
this
review,
we
present
comprehensive
summary
antifibrotic
roles
their
underlying
mechanisms
action.
As
food
derived
compound,
may
serve
promising
drug
candidate
Antioxidants and Redox Signaling,
Journal Year:
2017,
Volume and Issue:
27(13), P. 977 - 988
Published: May 31, 2017
This
review
evaluates
the
role
of
platelet-derived
transforming
growth
factor
(TGF)-β1
in
oxidative
stress-linked
pathologic
fibrosis,
with
an
emphasis
on
heart
and
kidney,
by
using
ionizing
radiation
as
a
clinically
relevant
stimulus.
Current
radiation-induced
organ
fibrosis
interventions
focus
pan-neutralization
TGF-β
or
use
anti-oxidants
anti-proliferative
agents,
limited
clinical
efficacy.
Recent
Advances:
Pathologic
represents
excessive
accumulation
collagen
other
extracellular
matrix
(ECM)
components
after
dysregulation
balance
between
ECM
synthesis
degradation.
Targets
based
endogenous
carbon
monoxide
(CO)
pathways
redox
modulators
such
N-acetylcysteine
present
promising
alternatives
to
current
therapeutic
regimens.Ionizing
leads
direct
DNA
damage
generation
reactive
oxygen
species
(ROS),
TGF-β1
activation
via
ROS,
thrombin
generation,
platelet
activation,
pro-inflammatory
signaling
promoting
myofibroblast
production.
Feed-forward
loops,
promotes
amplify
these
profibrotic
signals,
persistent
low-grade
inflammation
insures
their
perpetuation.
We
highlight
differential
roles
for
platelet-
versus
monocyte-derived
TGF-β1,
establishing
links
canonical
noncanonical
relationship
macrophage
polarization
autophagy,
define
points
where
pharmacologic
agents
can
intervene.Additional
studies
are
needed
understand
mechanisms
underlying
anti-fibrotic
effects
proposed
therapeutics,
limiting
activity,
promotion
polarization,
facilitation
autophagy.
Models
incorporating
CO
selective
that
impact
initiation
progression
including
nuclear
erythroid
2-related
(Nrf2)
redox,
particular
interest.
Antioxid.
Redox
Signal.
27,
977-988.
Stem Cell Research & Therapy,
Journal Year:
2020,
Volume and Issue:
11(1)
Published: June 26, 2020
Extracellular
vesicles
produced
by
bone
marrow
mesenchymal
stem
cells
(BMSC-EVs)
can
play
important
roles
in
the
repair
of
injured
tissues.
Though
numerous
studies
have
reported
effect
EVs
on
renal
fibrosis,
underlying
mechanisms
remain
unclear.
We
hypothesized
that
BMSC-EVs
containing
milk
fat
globule-epidermal
growth
factor-factor
8
(MFG-E8)
could
attenuate
fibrosis
inhibiting
RhoA/ROCK
pathway.We
investigated
whether
anti-fibrotic
effects
a
rat
model
which
rats
were
subjected
to
unilateral
ureteral
obstruction
(UUO),
as
well
cultured
HK2
cells.
from
BMSCs
collected
and
co-cultured
with
during
transforming
factor-β1
(TGF-β1)
treatment.
TGF-β1
also
treated
ROCK
inhibitor,
Y-27632.Compared
Sham
group,
UUO
displayed
fibrotic
abnormalities,
accompanied
an
increased
expression
α-smooth
muscle
actin
Fibronectin
reduced
E-cadherin.
These
molecular
pathological
changes
suggested
inflammation
damaged
kidneys.
Oxidative
stress,
evidenced
level
MDA
decreased
levels
SOD1
Catalase,
was
observed
Additionally,
activation
cleaved
caspase-3
PARP1
apoptosis
proximal
tubules
confirmed
tubular
cell
group.
All
these
phenotypes
exhibited
suppressed
treatment
BMSC-EVs.
However,
protective
completely
abolished
inhibition
MFG-E8.
Consistent
vivo
results,
inflammation,
oxidative
apoptosis,
HK-2
stimulated
vitro.
Interestingly,
Y-27632
protected
against
although
stress
unchanged.Our
results
show
MFG-E8
partly
through
pathway
inhibition.
Biomedicine & Pharmacotherapy,
Journal Year:
2021,
Volume and Issue:
143, P. 112115 - 112115
Published: Sept. 3, 2021
Renal
fibrosis
is
a
failed
wound-healing
process
of
the
kidney
tissue
after
chronic,
sustained
injury,
which
common
pathway
and
pathological
marker
virtually
every
type
chronic
disease
(CKD),
regardless
cause.
However,
there
lack
effective
treatment
specifically
targeting
against
renal
per
se
to
date.
The
main
feature
massive
activation
proliferation
fibroblasts
excessive
synthesis
secretion
extracellular
matrix
(ECM)
deposited
in
interstitium,
leading
structural
damage,
impairment
function,
eventually
end-stage
disease.
In
this
review,
we
summarize
recent
advancements
regarding
participation
interaction
many
types
residents
infiltrated
cells
during
fibrosis,
attempt
comprehensively
discuss
mechanism
from
cellular
level
conclude
by
highlighting
novel
therapeutic
targets
approaches
for
development
new
treatments
patients
with
fibrosis.
Oxidative Medicine and Cellular Longevity,
Journal Year:
2021,
Volume and Issue:
2021(1)
Published: Jan. 1, 2021
Fibrosis
is
the
final
common
pathology
of
most
chronic
diseases
as
seen
in
heart,
liver,
lung,
kidney,
and
skin
contributes
to
nearly
half
death
developed
countries.
Fibrosis,
or
scarring,
mainly
characterized
by
transdifferentiation
fibroblasts
into
myofibroblasts
excessive
accumulation
extracellular
matrix
(ECM)
secreted
myofibroblasts.
Despite
immense
efforts
made
field
organ
fibrosis
over
past
decades
considerable
understanding
occurrence
development
gained,
there
still
lack
an
effective
treatment
for
fibrotic
diseases.
Therefore,
identifying
a
new
therapeutic
strategy
against
unmet
clinical
need.
Naringenin,
flavonoid
that
occurs
naturally
citrus
fruits,
has
been
found
confer
wide
range
pharmacological
effects
including
antioxidant,
anti-inflammatory,
anticancer
benefits
thus
potentially
exerting
preventive
curative
on
numerous
In
addition,
emerging
evidence
revealed
naringenin
can
prevent
pathogenesis
vivo
vitro
via
regulation
various
pathways
involved
signaling
molecules
such
transforming
growth
factor-β1/small
mother
decapentaplegic
protein
3
(TGF-β1/Smad3),
mitogen-activated
kinase
(MAPK),
phosphatidylinositol
3-kinase/protein
B
(PI3K/Akt),
sirtuin1
(SIRT1),
nuclear
factor-kappa
(NF-κB),
reactive
oxygen
species
(ROS).
Targeting
these
profibrotic
could
become
novel
approach
management
disorders.
this
review,
we
present
comprehensive
summary
antifibrotic
roles
their
underlying
mechanisms
action.
As
food
derived
compound,
may
serve
promising
drug
candidate
