Journal of Translational Medicine,
Journal Year:
2023,
Volume and Issue:
21(1)
Published: Dec. 8, 2023
AMP-activated
protein
kinase
(AMPK)
is
a
ubiquitous
sensor
of
energy
and
nutritional
status
in
eukaryotic
cells.
It
plays
key
role
regulating
cellular
homeostasis
multiple
aspects
cell
metabolism.
During
macrophage
polarisation,
AMPK
not
only
guides
the
metabolic
programming
macrophages,
but
also
counter-regulates
inflammatory
function
macrophages
promotes
their
polarisation
toward
anti-inflammatory
phenotype.
located
at
intersection
metabolism
inflammation.
The
characteristics
are
closely
related
to
immune-related
diseases,
infectious
cancer
progression
immunotherapy.
This
review
discusses
structure
its
metabolism,
macrophages.
In
addition,
it
summarises
important
pathway
activators
development
macrophage-related
diseases.
Free Radical Biology and Medicine,
Journal Year:
2020,
Volume and Issue:
152, P. 116 - 141
Published: March 8, 2020
Nonalcoholic
fatty
liver
disease
(NAFLD)
has
emerged
as
the
most
common
chronic
worldwide
and
is
strongly
associated
with
presence
of
oxidative
stress.
Disturbances
in
lipid
metabolism
lead
to
hepatic
accumulation,
which
affects
different
reactive
oxygen
species
(ROS)
generators,
including
mitochondria,
endoplasmic
reticulum,
NADPH
oxidase.
Mitochondrial
function
adapts
NAFLD
mainly
through
downregulation
electron
transport
chain
(ETC)
preserved
or
enhanced
capacity
mitochondrial
acid
oxidation,
stimulates
ROS
overproduction
within
ETC
components
upstream
cytochrome
c
However,
non-ETC
sources
ROS,
particular,
β-oxidation,
appear
produce
more
metabolic
diseases.
Endoplasmic
reticulum
stress
oxidase
alterations
are
also
NAFLD,
but
degree
their
contribution
remains
unclear.
Increased
generation
induces
changes
insulin
sensitivity
expression
activity
key
enzymes
involved
metabolism.
Moreover,
interaction
between
redox
signaling
innate
immune
forms
a
complex
network
that
regulates
inflammatory
responses.
Based
on
mechanistic
view
described
above,
this
review
summarizes
mechanisms
may
account
for
excessive
production
potential
roles
drive
progression,
therapeutic
interventions
related
International Immunology,
Journal Year:
2018,
Volume and Issue:
30(11), P. 511 - 528
Published: Aug. 22, 2018
Abstract
Tissue
injury
triggers
a
complex
series
of
cellular
responses,
starting
from
inflammation
activated
by
tissue
and
cell
damage
proceeding
to
healing.
By
clearing
debris,
activating
resolving
promoting
fibrosis,
macrophages
play
key
roles
in
most,
if
not
all,
phases
the
response
injury.
Recent
studies
mechanisms
underlying
initial
later
regeneration
repair
revealed
that
bridge
these
processes
part
supporting
stem/progenitor
cells,
damaged
tissue,
remodeling
extracellular
matrix
prepare
scaffolding
for
angiogenesis.
However,
also
have
central
role
development
pathology
induced
failed
resolution
(e.g.
chronic
inflammation)
excessive
scarring.
In
this
review,
we
summarize
activities
healing
acute
tissues
with
differing
regenerative
capacities.
While
lead
similar
tissues,
their
priorities
consequences
differ
among
tissues.
Moreover,
magnitude,
nature
duration
greatly
affect
responses
processes.
particular,
continuous
and/or
leads
ailments
which
macrophage
may
become
detrimental.
Lipids in Health and Disease,
Journal Year:
2017,
Volume and Issue:
16(1)
Published: Oct. 16, 2017
Nonalcoholic
fatty
liver
disease
(NAFLD)
comprises
a
spectrum
of
diseases,
including
simple
steatosis,
nonalcoholic
steatohepatitis
(NASH),
cirrhosis
and
hepatocellular
carcinoma.
Lipotoxicity,
insulin
resistance
(IR)
inflammation
are
involved
in
the
process.
Lipotoxicity
promotes
IR,
which
turn,
increase
adipocyte
lipolysis
exacerbates
lipotoxicity.
Furthermore,
IR
form
vicious
circle,
with
each
condition
promoting
other
accelerating
development
NAFLD
presence
As
an
integrator
inflammatory
pathway
networks,
nuclear
factor-kappa
B
(NF-κB)
regulates
expression
pro-inflammatory
cytokines,
such
as
tumor
necrosis
factor-alpha
(TNF-α),
interleukin
6
(IL-6),
anti-inflammatory
adiponectin
NAFLD.
In
this
review,
relationships
between
lipotoxicity,
discussed,
particular
emphasis
on
pathways.
Cell Reports,
Journal Year:
2019,
Volume and Issue:
26(1), P. 192 - 208.e6
Published: Jan. 1, 2019
The
AMP-activated
protein
kinase
(AMPK)
is
a
highly
conserved
master
regulator
of
metabolism,
whose
activation
has
been
proposed
to
be
therapeutically
beneficial
for
the
treatment
several
metabolic
diseases,
including
nonalcoholic
fatty
liver
disease
(NAFLD).
NAFLD,
characterized
by
excessive
accumulation
hepatic
lipids,
most
common
chronic
and
major
risk
factor
development
steatohepatitis,
type
2
diabetes,
other
conditions.
To
assess
therapeutic
potential
AMPK
activation,
we
have
generated
genetically
engineered
mouse
model,
termed
iAMPKCA,
where
can
inducibly
activated
in
vivo
mice
spatially
temporally
restricted
manner.
Using
this
show
that
liver-specific
reprograms
lipid
reduces
steatosis,
decreases
expression
inflammation
fibrosis
genes,
leads
significant
benefits
context
diet-induced
obesity.
These
findings
further
support
as
target
prevention
NAFLD.
Frontiers in Physiology,
Journal Year:
2018,
Volume and Issue:
9
Published: Feb. 21, 2018
Obesity
occurs
when
excess
energy
accumulates
in
white
adipose
tissue
(WAT),
whereas
brown
(BAT),
which
is
specialized
dissipating
through
thermogenesis,
potently
counteracts
obesity.
White
adipocytes
can
be
converted
to
thermogenic
"brown-like"
cells
(beige
cells;
WAT
browning)
under
various
stimuli,
such
as
cold
exposure.
AMP-activated
protein
kinase
(AMPK)
a
crucial
sensor
that
regulates
metabolism
multiple
tissues.
However,
the
role
of
AMPK
function,
especially
browning
process,
not
fully
understood.
To
illuminate
effect
adipocyte
on
metabolism,
we
generated
Adiponectin-Cre-driven
tissue-specific
α1/α2
KO
mice
(AKO).
These
AKO
were
intolerant
and
their
inguinal
displayed
impaired
mitochondrial
integrity
biogenesis,
reduced
expression
markers
upon
High-fat-diet
(HFD)-fed
exhibited
increased
adiposity
exacerbated
hepatic
steatosis
fibrosis
glucose
tolerance
insulin
sensitivity.
Meanwhile,
expenditure
oxygen
consumption
markedly
decreased
both
basal
conditions
after
stimulation
with
β3-adrenergic
receptor
agonist,
CL
316,243.
In
contrast,
found
HFD-fed
obese
mouse
model,
chronic
activation
by
A-769662
protected
against
obesity
related
metabolic
dysfunction.
alleviated
HFD-induced
intolerance
body
weight
gain
expansion.
Notably,
mice.
treatment
also
induced
process
fat
depot
Likewise,
enhanced
thermogenesis
differentiated
stromal
vascular
fraction
(SVF)
via
signaling
pathway.
summary,
lack
AMPKα
impairment
response
nutrient-overload,
respectively,
promoted
findings
reveal
vital
for
regulating
maintaining
homeostasis,
suggests
targeted
may
promising
strategy
anti-obesity
therapy.
