Seminars in Immunology,
Journal Year:
2016,
Volume and Issue:
28(5), P. 514 - 524
Published: Oct. 1, 2016
Recent
advances
in
the
field
of
immunometabolism
support
concept
that
fundamental
processes
T
cell
biology,
such
as
TCR-mediated
activation
and
helper
lineage
differentiation,
are
closely
linked
to
changes
cellular
metabolic
programs.
Although
major
task
intermediate
metabolism
is
provide
with
a
constant
supply
energy
molecular
precursors
for
production
biomolecules,
dynamic
regulation
pathways
also
plays
an
active
role
shaping
responses.
Key
glycolysis,
fatty
acid
mitochondrial
now
recognized
crucial
players
their
modulation
can
differentially
affect
development
lineages.
In
this
review,
we
describe
diverse
cells
engage
during
life
cycle
from
naïve
towards
effector
memory
cells.
We
consider
particular
how
may
actively
function
different
states.
Moreover,
discuss
regulators
mTOR
or
AMPK
link
environmental
adaptations
elucidate
consequences
on
differentiation
function.
Gut,
Journal Year:
2019,
Volume and Issue:
69(7), P. 1193 - 1205
Published: Oct. 3, 2019
Objective
N
6
-methyladenosine
(m
A)
RNA
methylation
and
its
associated
methyltransferase
METTL3
are
involved
in
tumour
initiation
progression
via
the
regulation
of
function.
This
study
explored
biological
function
clinical
significance
gastric
cancer
(GC).
Design
The
prognostic
value
expression
was
evaluated
using
tissue
microarray
immunohistochemical
staining
analyses
a
human
GC
cohort.
role
mechanism
growth
liver
metastasis
were
determined
vitro
vivo.
Results
level
m
A
significantly
increased
GC,
main
regulator
abundant
modification.
elevated
tissues
with
poor
prognosis.
Multivariate
Cox
regression
analysis
revealed
that
an
independent
factor
effective
predictor
patients
GC.
Moreover,
overexpression
promoted
proliferation
Mechanistically,
P300-mediated
H3K27
acetylation
activation
promoter
induced
transcription,
which
stimulated
modification
HDGF
mRNA,
reader
IGF2BP3
then
directly
recognised
bound
to
site
on
mRNA
enhanced
stability.
Secreted
angiogenesis,
while
nuclear
activated
GLUT4
ENO2
expression,
followed
by
increase
glycolysis
cells,
correlated
subsequent
metastasis.
Conclusions
Elevated
promotes
angiogenesis
indicating
is
potential
biomarker
therapeutic
target
for
Molecular Cancer,
Journal Year:
2017,
Volume and Issue:
16(1)
Published: April 13, 2017
Cancer
cells
are
frequently
confronted
with
metabolic
stress
in
tumor
microenvironments
due
to
their
rapid
growth
and
limited
nutrient
supply.
Metabolic
induces
cell
death
through
ROS-induced
apoptosis.
However,
cancer
can
adapt
it
by
altering
the
pathways.
AMPK
AKT
two
primary
effectors
response
stress:
acts
as
an
energy-sensing
factor
which
rewires
metabolism
maintains
redox
balance.
broadly
promotes
energy
production
abundance
milieu,
but
role
of
under
is
dispute.
Recent
studies
show
that
display
antagonistic
roles
stress.
stress-induced
ROS
signaling
lies
hub
between
reprogramming
homeostasis.
Here,
we
highlight
cross-talk
regulation
on
elimination,
summarizes
mechanism
adaptability
suggests
potential
options
for
therapeutics.
International Journal of Molecular Sciences,
Journal Year:
2019,
Volume and Issue:
20(13), P. 3177 - 3177
Published: June 28, 2019
Cancer
is
a
problem
with
worldwide
importance
and
the
second
leading
cause
of
death
globally.
cells
reprogram
their
metabolism
to
support
uncontrolled
expansion
by
increasing
biomass
(anabolic
metabolism—glycolysis)
at
expense
energy
(bioenergetics-mitochondrial
function)
requirements.
In
this
aspect,
metabolic
reprogramming
stands
out
as
key
biological
process
in
understanding
conversion
normal
cell
into
neoplastic
precursor.
Quercetin
major
representative
flavonoid
subclass
flavonols.
ubiquitously
present
fruits
vegetables,
being
one
most
common
dietary
flavonols
western
diet.
The
anti-cancer
effects
quercetin
include
its
ability
promote
loss
viability,
apoptosis
autophagy
through
modulation
PI3K/Akt/mTOR,
Wnt/β-catenin,
MAPK/ERK1/2
pathways.
review,
we
discuss
role
cancer
metabolism,
addressing
specifically
target
molecular
pathways
involved
glucose
mitochondrial
function.
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.
Frontiers in Cell and Developmental Biology,
Journal Year:
2019,
Volume and Issue:
7
Published: Jan. 29, 2019
While
oxygen
is
critical
to
the
continued
existence
of
complex
organisms,
extreme
levels
within
a
system,
known
as
hypoxia
(low
oxygen)
and
hyperoxia
(excessive
oxygen),
potentially
promote
stress
defined
biological
environment.
The
consequences
tissue
hypoxia,
result
defective
supply,
vary
in
response
gravity,
extent
environment
malfunction.
Persistent
pathological
incompatible
with
normal
functions,
result,
multicellular
organisms
have
been
compelled
develop
both
organism-wide
cellular-level
solutions.
Both
direct,
including
oxidative
phosphorylation
down-regulation
inhibition
fatty-acid
desaturation,
indirect
processes,
altered
hypoxia-sensitive
transcription
factor
expression,
facilitate
metabolic
modifications
that
occur
hypoxia.
Due
dysfunctional
vasculature
associated
large
areas
some
cancers,
sections
these
tumours
continue
hypoxic
environments.
Crucial
drug
development,
robust
understanding
significance
metabolism
changes
will
our
cancer
cell
survival.
This
review
defines
current
knowledge
base
several
hypoxia-instigated
exemplifies
correlation
between
change
its
support
hypoxic-adapted
malignancy.
Frontiers in Immunology,
Journal Year:
2018,
Volume and Issue:
9
Published: May 16, 2018
Immune
cell
function
and
metabolism
are
closely
linked.
Many
studies
have
now
clearly
demonstrated
that
alterations
in
cellular
influence
immune
that,
conversely,
determines
the
metabolic
state.
Less
well
understood,
however,
effects
of
systemic
or
whole
organism
nutritional
status
on
metabolism.
Several
undernutrition
is
associated
with
immunosuppression,
which
leads
to
both
increased
susceptibility
infection
protection
against
several
types
autoimmune
disease,
whereas
overnutrition
low-grade,
chronic
inflammation
increases
risk
cardiovascular
promotes
autoreactivity,
disrupts
protective
immunity.
Here,
we
review
immunity
highlight
nutrition
circulating
cytokines
populations
human
mouse
models.
As
T
cells
critical
members
system,
direct
overall
response,
will
focus
this
function.
hormones
been
identified
mediate
through
expression
action
key
regulatory
signaling
proteins.
Understanding
how
sensitive
inadequate
overabundant
nutrients
may
enhance
our
ability
target
alter
malnutrition
obesity.
