Frontiers in Oncology,
Journal Year:
2019,
Volume and Issue:
9
Published: Aug. 8, 2019
Endometrial
cancer
is
one
of
the
most
common
cancers
female
reproductive
system.
Although
surgery,
radiotherapy,
chemotherapy
and
hormone
therapy
can
significantly
improve
survival
patients,
treatment
patients
with
very
early
lesions
a
strong
desire
to
retain
function
or
late
recurrence
still
in
stages.
Metabolic
syndrome
(MS)
clustering
at
least
three
five
following
medical
conditions:
central
obesity,
high
blood
pressure,
sugar,
serum
triglycerides,
low
high-density
lipoprotein
(HDL).
Obesity,
diabetes
hypertension
often
coexist
endometrial
cancer,
which
increases
risk
also
known
as
"triple
cancer".
In
recent
years,
epidemiological
clinical
studies
have
found
that
MS
associated
metabolic
diseases
closely
related
incidence
cancer.
However,
key
molecular
mechanisms
underlying
induction
by
not
been
elucidated
date.
Characterizing
tumor
metabolism
microenvironment
will
be
advantageous
for
achieving
comprehensive
view
mechanism
providing
new
target
This
review
focuses
on
advances
determining
role
syndrome-related
factors
pathogenesis
We
suggest
interfering
microenvironment-related
signals
may
inhibit
occurrence
International Journal of Molecular Sciences,
Journal Year:
2020,
Volume and Issue:
21(7), P. 2632 - 2632
Published: April 10, 2020
Lipotoxicity
is
characterized
by
the
ectopic
accumulation
of
lipids
in
organs
different
from
adipose
tissue.
mainly
associated
with
dysfunctional
signaling
and
insulin
resistance
response
non-adipose
tissue
such
as
myocardium,
pancreas,
skeletal
muscle,
liver,
kidney.
Serum
lipid
abnormalities
renal
have
been
development
kidney
diseases,
particular
diabetic
nephropathy.
Chronic
hyperinsulinemia,
often
seen
type
2
diabetes,
plays
a
crucial
role
blood
liver
metabolism
abnormalities,
thus
resulting
increased
non-esterified
fatty
acids
(NEFA).
Excessive
alters
cellular
homeostasis
activates
lipogenic
glycogenic
cell-signaling
pathways.
Recent
evidences
indicate
that
both
quantity
quality
are
involved
damage
to
lipotoxicity
activating
inflammation,
oxidative
stress,
mitochondrial
dysfunction,
cell-death.
The
pathological
effects
observed
cells,
promoting
podocyte
injury,
tubular
damage,
mesangial
proliferation,
endothelial
activation,
formation
macrophage-derived
foam
cells.
Therefore,
this
review
examines
recent
preclinical
clinical
research
about
potentially
harmful
kidney,
metabolic
markers
these
mechanisms,
major
pathways
affected,
causes
excessive
accumulation,
types
involved,
well
offers
comprehensive
update
therapeutic
strategies
targeting
lipotoxicity.
Journal of Clinical Medicine,
Journal Year:
2020,
Volume and Issue:
9(1), P. 253 - 253
Published: Jan. 17, 2020
Ischemia
and
reperfusion
injury
(IRI)
is
a
complex
pathophysiological
phenomenon,
inevitable
in
kidney
transplantation
one
of
the
most
important
mechanisms
for
non-
or
delayed
function
immediately
after
transplantation.
Long
term,
it
associated
with
acute
rejection
chronic
graft
dysfunction
due
to
interstitial
fibrosis
tubular
atrophy.
Recently,
more
insight
has
been
gained
underlying
molecular
pathways
signalling
cascades
involved,
which
opens
door
new
therapeutic
opportunities
aiming
reduce
IRI
improve
survival.
This
review
systemically
discusses
specific
involved
pathophysiology
highlights
strategies
targeting
these
pathways.
Signal Transduction and Targeted Therapy,
Journal Year:
2022,
Volume and Issue:
7(1)
Published: June 9, 2022
Abstract
Chronic
kidney
disease
(CKD)
is
a
chronic
renal
dysfunction
syndrome
that
characterized
by
nephron
loss,
inflammation,
myofibroblasts
activation,
and
extracellular
matrix
(ECM)
deposition.
Lipotoxicity
oxidative
stress
are
the
driving
force
for
loss
of
including
tubules,
glomerulus,
endothelium.
NLRP3
inflammasome
signaling,
MAPK
PI3K/Akt
RAAS
signaling
involves
in
lipotoxicity.
The
upregulated
Nox
expression
decreased
Nrf2
result
directly.
injured
resident
cells
release
proinflammatory
cytokines
chemokines
to
recruit
immune
such
as
macrophages
from
bone
marrow.
NF-κB
JAK-STAT
Toll-like
receptor
cGAS-STING
major
pathways
mediate
inflammation
inflammatory
cells.
produce
secret
great
number
profibrotic
TGF-β1,
Wnt
ligands,
angiotensin
II.
TGF-β
Notch
evoke
activation
promote
generation
ECM.
potential
therapies
targeted
these
also
introduced
here.
In
this
review,
we
update
key
lipotoxicity,
stress,
kidneys
with
injury,
drugs
based
on
latest
studies.
Unifying
will
be
instrumental
advance
further
basic
clinical
investigation
CKD.
Journal of the American Society of Nephrology,
Journal Year:
2017,
Volume and Issue:
28(10), P. 2856 - 2865
Published: Aug. 4, 2017
AKI
is
associated
with
high
morbidity
and
mortality,
it
predisposes
to
the
development
progression
of
CKD.
Novel
strategies
that
minimize
halt
CKD
are
urgently
needed.
Normal
kidney
function
involves
numerous
different
cell
types,
such
as
tubular
epithelial
cells,
endothelial
podocytes,
working
in
concert.
This
delicate
balance
many
energy-intensive
processes.
Fatty
acids
preferred
energy
substrates
for
kidney,
defects
fatty
acid
oxidation
mitochondrial
dysfunction
universally
involved
diverse
causes
review
provides
an
overview
ATP
production
demands
summarizes
preclinical
clinical
evidence
New
therapeutic
targeting
mitochondria
protection
cellular
bioenergetics
presented,
emphasis
on
those
have
been
evaluated
animal
models
Targeting
upstream
damage
may
offer
advantages
compared
downstream
inflammatory
fibrosis
International Journal of Molecular Sciences,
Journal Year:
2021,
Volume and Issue:
22(20), P. 11253 - 11253
Published: Oct. 19, 2021
Mitochondria
are
heterogeneous
and
highly
dynamic
organelles,
playing
critical
roles
in
adenosine
triphosphate
(ATP)
synthesis,
metabolic
modulation,
reactive
oxygen
species
(ROS)
generation,
cell
differentiation
death.
Mitochondrial
dysfunction
has
been
recognized
as
a
contributor
many
diseases.
The
kidney
is
an
organ
enriched
mitochondria
with
high
energy
demand
the
human
body.
Recent
studies
have
focusing
on
how
mitochondrial
contributes
to
pathogenesis
of
different
forms
diseases,
including
acute
injury
(AKI)
chronic
disease
(CKD).
AKI
linked
increased
risk
developing
CKD.
CKD
broad
clinical
syndrome
substantial
impact
morbidity
mortality,
encompassing
various
etiologies
representing
important
challenges
for
global
public
health.
Renal
disorders
common
feature
diverse
CKD,
which
result
from
defects
structure,
dynamics,
biogenesis
well
crosstalk
other
organelles.
Persistent
dysregulation
homeostasis
affects
cellular
pathways,
leading
increase
renal
microvascular
loss,
oxidative
stress,
apoptosis,
eventually
failure.
It
understand
molecular
events
that
govern
functions
pathophysiology
should
facilitate
development
novel
therapeutic
strategies.
This
review
provides
overview
insights
specific
pathogenic
mechanisms
progression
AKI,
transition.
We
also
discuss
possible
beneficial
effects
mitochondrial-targeted
agents
treatment
dysfunction-mediated
may
translate
into
options
ameliorate
delay
these
Clinical Science,
Journal Year:
2022,
Volume and Issue:
136(7), P. 493 - 520
Published: April 1, 2022
Abstract
Albuminuria
is
the
hallmark
of
both
primary
and
secondary
proteinuric
glomerulopathies,
including
focal
segmental
glomerulosclerosis
(FSGS),
obesity-related
nephropathy,
diabetic
nephropathy
(DN).
Moreover,
albuminuria
an
important
feature
all
chronic
kidney
diseases
(CKDs).
Podocytes
play
a
key
role
in
maintaining
permselectivity
glomerular
filtration
barrier
(GFB)
injury
podocyte,
leading
to
foot
process
(FP)
effacement
podocyte
loss,
unifying
underlying
mechanism
glomerulopathies.
The
metabolic
insult
hyperglycemia
paramount
importance
pathogenesis
DN,
while
insults
damage
are
poorly
defined
other
However,
shared
mechanisms
have
been
identified.
Herein,
we
will
review
haemodynamic
oxidative
stress,
inflammation,
lipotoxicity,
endocannabinoid
(EC)
hypertone,
mitochondrial
autophagic
dysfunction
damage,
focussing
particularly
on
their
DN.
Gaining
better
insight
into
may
provide
novel
targets
for
treatment.
strategies
boosting
repair
open
way
regenerative
medicine.
