Clinical and Molecular Hepatology,
Journal Year:
2022,
Volume and Issue:
29(1), P. 77 - 98
Published: Oct. 13, 2022
The
initial
presentation
of
non-alcoholic
steatohepatitis
(NASH)
is
hepatic
steatosis.
dysfunction
lipid
metabolism
within
hepatocytes
caused
by
genetic
factors,
diet,
and
insulin
resistance
causes
accumulation.
Lipotoxicity,
oxidative
stress,
mitochondrial
dysfunction,
endoplasmic
reticulum
stress
would
further
contribute
to
hepatocyte
injury
death,
leading
inflammation
immune
in
the
liver.
During
healing
process,
accumulation
an
excessive
amount
fibrosis
might
occur
while
healing.
development
NASH
liver
fibrosis,
gut-liver
axis,
adipose-liver
renin-angiotensin
system
(RAS)
may
be
dysregulated
impaired.
Translocation
bacteria
or
its
end-products
entering
could
activate
hepatocytes,
Kupffer
cells,
stellate
exacerbating
steatosis,
inflammation,
fibrosis.
Bile
acids
regulate
glucose
through
Farnesoid
X
receptors
intestine.
Increased
adipose
tissue-derived
non-esterified
fatty
aggravate
leptin
also
plays
a
role
fibrogenesis,
decreased
adiponectin
resistance.
Moreover,
dysregulation
peroxisome
proliferator-activated
liver,
adipose,
muscle
tissues
impair
metabolism.
In
addition,
RAS
acid
metabolism,
treatment
includes
lifestyle
modification,
pharmacological
therapy,
non-pharmacological
therapy.
Currently,
weight
reduction
modification
surgery
most
effective
However,
vitamin
E,
pioglitazone,
obeticholic
have
been
suggested.
this
review,
we
will
introduce
some
new
clinical
trials
experimental
therapies
for
related
British Journal of Cancer,
Journal Year:
2019,
Volume and Issue:
122(1), P. 4 - 22
Published: Dec. 10, 2019
Abstract
A
common
feature
of
cancer
cells
is
their
ability
to
rewire
metabolism
sustain
the
production
ATP
and
macromolecules
needed
for
cell
growth,
division
survival.
In
particular,
importance
altered
fatty
acid
in
has
received
renewed
interest
as,
aside
principal
role
as
structural
components
membrane
matrix,
they
are
important
secondary
messengers,
can
also
serve
fuel
sources
energy
production.
this
review,
we
will
examine
mechanisms
through
which
with
a
focus
on
four
main
areas
research.
(1)
The
de
novo
synthesis
exogenous
uptake
cellular
pool
acids.
(2)
molecular
heterogeneity
oncogenic
signal
transduction
pathways,
such
PI3K–AKT–mTOR
signalling,
regulate
metabolism.
(3)
acids
essential
mediators
progression
metastasis,
remodelling
tumour
microenvironment.
(4)
Therapeutic
strategies
considerations
successfully
targeting
cancer.
Further
research
focusing
complex
interplay
between
signalling
dysregulated
holds
great
promise
uncover
novel
metabolic
vulnerabilities
improve
efficacy
targeted
therapies.
Cell & Bioscience,
Journal Year:
2020,
Volume and Issue:
10(1)
Published: March 10, 2020
Abstract
Mammalian
target
of
rapamycin
(mTOR)
regulates
cell
proliferation,
autophagy,
and
apoptosis
by
participating
in
multiple
signaling
pathways
the
body.
Studies
have
shown
that
mTOR
pathway
is
also
associated
with
cancer,
arthritis,
insulin
resistance,
osteoporosis,
other
diseases.
The
pathway,
which
often
activated
tumors,
not
only
gene
transcription
protein
synthesis
to
regulate
proliferation
immune
differentiation
but
plays
an
important
role
tumor
metabolism.
Therefore,
a
hot
anti-tumor
therapy
research.
In
recent
years,
variety
newly
discovered
inhibitors
entered
clinical
studies,
drugs
been
proven
high
activity
combination
inhibitors.
purpose
this
review
introduce
on
apoptosis,
growth,
metabolism
cells,
research
progress
field.
Physiological Reviews,
Journal Year:
2021,
Volume and Issue:
101(3), P. 1371 - 1426
Published: Feb. 18, 2021
Cells
metabolize
nutrients
for
biosynthetic
and
bioenergetic
needs
to
fuel
growth
proliferation.
The
uptake
of
from
the
environment
their
intracellular
metabolism
is
a
highly
controlled
process
that
involves
cross
talk
between
signaling
metabolic
pathways.
Despite
constant
fluctuations
in
nutrient
availability
environmental
signals,
normal
cells
restore
homeostasis
maintain
cellular
functions
prevent
disease.
A
central
molecule
integrates
with
mechanistic
target
rapamycin
(mTOR).
mTOR
protein
kinase
responds
levels
signals.
forms
two
complexes,
mTORC1,
which
sensitive
rapamycin,
mTORC2,
not
directly
inhibited
by
this
drug.
Rapamycin
has
facilitated
discovery
various
mTORC1
metabolism.
Genetic
models
disrupt
either
or
mTORC2
have
expanded
our
knowledge
cellular,
tissue,
as
well
systemic
Nevertheless,
regulation
particularly
metabolism,
lagged
behind.
Since
an
important
cancer,
aging,
other
metabolism-related
pathologies,
understanding
distinct
overlapping
complexes
vital
development
more
effective
therapeutic
strategies.
This
review
discusses
key
discoveries
recent
findings
on
complexes.
We
highlight
cancer
but
also
discuss
examples
mTOR-mediated
reprogramming
occurring
stem
immune
cells,
type
2
diabetes/obesity,
neurodegenerative
disorders,
aging.
Cell Death and Disease,
Journal Year:
2020,
Volume and Issue:
11(2)
Published: Feb. 6, 2020
Lipid
droplets
(also
known
as
lipid
bodies)
are
lipid-rich,
cytoplasmic
organelles
that
play
important
roles
in
cell
signaling,
metabolism,
membrane
trafficking,
and
the
production
of
inflammatory
mediators.
droplet
biogenesis
is
a
regulated
process,
accumulation
these
within
leukocytes,
epithelial
cells,
hepatocytes,
other
nonadipocyte
cells
frequently
observed
phenotype
several
physiologic
or
pathogenic
situations
thoroughly
described
during
conditions.
Moreover,
recent
years,
studies
have
an
increase
intracellular
different
neoplastic
processes,
although
it
not
clear
whether
directly
involved
establishment
types
malignancies.
This
review
discusses
current
evidence
related
to
biogenesis,
composition
functions
hallmarks
cancer:
inflammation,
increased
proliferation,
escape
from
death,
hypoxia.
potential
markers
disease
targets
for
novel
anti-inflammatory
antineoplastic
therapies
will
be
discussed.
Acta Pharmaceutica Sinica B,
Journal Year:
2021,
Volume and Issue:
12(2), P. 558 - 580
Published: Sept. 27, 2021
Hepatocellular
carcinoma
(HCC)
is
an
aggressive
human
cancer
with
increasing
incidence
worldwide.
Multiple
efforts
have
been
made
to
explore
pharmaceutical
therapies
treat
HCC,
such
as
targeted
tyrosine
kinase
inhibitors,
immune
based
and
combination
of
chemotherapy.
However,
limitations
exist
in
current
strategies
including
chemoresistance
for
instance.
Tumor
initiation
progression
driven
by
reprogramming
metabolism,
particular
during
HCC
development.
Recently,
metabolic
associated
fatty
liver
disease
(MAFLD),
a
reappraisal
new
nomenclature
non-alcoholic
(NAFLD),
indicates
growing
appreciation
metabolism
the
pathogenesis
disease,
thereby
suggesting
targeting
abnormal
treatment.
In
this
review,
we
introduce
directions
highlighting
targets
glucose,
acid,
amino
acid
glutamine
which
are
suitable
intervention.
We
also
summarize
discuss
agents
studies
deregulated
Furthermore,
opportunities
challenges
discovery
development
therapy
discussed.
