BMC Nephrology,
Journal Year:
2020,
Volume and Issue:
21(1)
Published: July 13, 2020
Abstract
Chronic
kidney
disease
(CKD)
is
characterized
by
inflammation,
injury
and
fibrosis.
Dysregulated
innate
immune
responses
mediated
macrophages
play
critical
roles
in
progressive
renal
injury.
The
differentiation
polarization
of
into
pro-inflammatory
‘M1’
anti-inflammatory
‘M2’
states
represent
the
two
extreme
maturation
programs
during
tissue
However,
effects
macrophage
on
pathogenesis
CKD
are
not
fully
understood.
In
this
review,
we
discuss
mechanisms
underlying
role
initiation,
progression,
resolution
recurrence
CKD.
Macrophage
activation
initiated
through
recognition
conserved
endogenous
exogenous
molecular
motifs
pattern
receptors,
chiefly,
Toll-like
receptors
(TLRs),
which
located
cell
surface
endosomes,
NLR
inflammasomes,
positioned
cytosol.
Recent
data
suggest
that
genetic
variants
molecule
apolipoprotein
L1
(APOL1)
associated
with
increased
prevalence
people
African
descent,
mediate
an
atypical
M1
polarization.
Manipulation
may
offer
novel
strategies
to
address
dysregulated
immunometabolism
provide
a
complementary
approach
along
current
podocentric
treatment
for
glomerular
diseases.
Frontiers in Immunology,
Journal Year:
2023,
Volume and Issue:
14
Published: April 4, 2023
The
physiological
processes
of
cell
growth,
proliferation,
differentiation,
and
apoptosis
are
closely
related
to
STAT3,
it
has
been
demonstrated
that
aberrant
STAT3
expression
an
impact
on
the
onset
progression
a
number
inflammatory
immunological
disorders,
fibrotic
diseases,
malignancies.
In
order
produce
necessary
biological
effects,
macrophages
(M0)
can
be
polarized
into
pro-inflammatory
(M1)
anti-inflammatory
(M2)
types
in
response
various
microenvironmental
stimuli.
signaling
is
involved
macrophage
polarization,
research
effect
polarization
gained
attention
recent
years.
provide
references
for
treatment
investigation
disorders
this
review
compiles
pertinent
pathways
associated
with
from
many
fundamental
studies.
Frontiers in Immunology,
Journal Year:
2022,
Volume and Issue:
13
Published: Oct. 6, 2022
As
the
essential
regulators
of
organ
fibrosis,
macrophages
undergo
marked
phenotypic
and
functional
changes
after
injury.
These
in
macrophage
phenotype
function
can
result
maladaptive
repair,
causing
chronic
inflammation
development
pathological
fibrosis.
Autophagy,
a
highly
conserved
lysosomal
degradation
pathway,
is
one
major
players
to
maintain
homeostasis
through
clearing
protein
aggregates,
damaged
organelles,
invading
pathogens.
Emerging
evidence
has
shown
that
autophagy
plays
an
role
polarization,
inflammation,
Because
high
heterogeneity
different
organs,
types
may
play
roles
Here,
we
review
current
understanding
fibrosis
highlight
potential
treatment
Finally,
important
unresolved
issues
this
field
are
briefly
discussed.
A
better
mechanisms
contribute
developing
novel
therapies
for
inflammatory
diseases
Antioxidants,
Journal Year:
2023,
Volume and Issue:
12(2), P. 239 - 239
Published: Jan. 20, 2023
Reducing
oxidative
stress
stands
at
the
center
of
a
prevention
and
control
strategy
for
mitigating
cellular
senescence
aging.
Kidney
disease
is
characterized
by
premature
aging
syndrome,
to
find
modulator
targeting
against
stress,
mitochondrial
dysfunction,
in
kidney
cells
could
be
great
significance
prevent
progression
this
disease.
This
review
focuses
on
pathogenic
mechanisms
related
appearance
damage
dysfunction
In
scenario,
anti-aging
Klotho
protein
plays
crucial
role
modulating
signaling
pathways
involving
manganese-containing
superoxide
dismutase
(Mn-SOD)
transcription
factors
FoxO
Nrf2,
known
antioxidant
systems,
other
function
regulators,
such
as
uncoupling
1
(UCP1),
B-cell
lymphoma-2
(BCL-2),
Wnt/β-catenin,
peroxisome
proliferator-activated
receptor
gamma
coactivator
1-alpha
(PGC-1
alpha),
factor
EB,
(TFEB),
(PPAR-gamma).
Therefore,
postulated
very
promising
new
target
future
therapeutic
strategies
mitochondria
abnormalities,
patients.
Journal of Translational Medicine,
Journal Year:
2023,
Volume and Issue:
21(1)
Published: Oct. 9, 2023
Abstract
Cancer
remains
the
leading
cause
of
death
around
world.
In
cancer
treatment,
over
50%
patients
receive
radiotherapy
alone
or
in
multimodal
combinations
with
other
therapies.
One
adverse
consequences
after
radiation
exposure
is
occurrence
radiation-induced
tissue
fibrosis
(RIF),
which
characterized
by
abnormal
activation
myofibroblasts
and
excessive
accumulation
extracellular
matrix.
This
phenotype
can
manifest
multiple
organs,
such
as
lung,
skin,
liver
kidney.
In-depth
studies
on
mechanisms
have
shown
that
a
variety
signals
immune
cells
release
cytokines,
intracellular
cGAS/STING,
oxidative
stress
response,
metabolic
reprogramming
proteasome
pathway
are
involved
myofibroblasts.
Tissue
extremely
harmful
to
patients'
health
requires
early
diagnosis.
addition
traditional
serum
markers,
histologic
imaging
tests,
diagnostic
potential
nuclear
medicine
techniques
emerging.
Anti-inflammatory
antioxidant
therapies
treatments
for
fibrosis.
Recently,
some
promising
therapeutic
strategies
emerged,
stem
cell
therapy
targeted
However,
incomplete
knowledge
hinders
treatment
this
disease.
Here,
we
also
highlight
mechanistic,
directions
MedComm,
Journal Year:
2023,
Volume and Issue:
4(5)
Published: Sept. 11, 2023
Abstract
Macrophages
play
diverse
roles
in
development,
homeostasis,
and
immunity.
Accordingly,
the
dysfunction
of
macrophages
is
involved
occurrence
progression
various
diseases,
such
as
coronavirus
disease
2019
atherosclerosis.
The
protective
or
pathogenic
effect
that
exert
different
conditions
largely
depends
on
their
functional
plasticity,
which
regulated
via
signal
transduction
Janus
kinase–signal
transducer
activator
transcription,
Wnt
Notch
pathways,
stimulated
by
environmental
cues.
Over
past
few
decades,
molecular
mechanisms
signaling
pathways
have
been
gradually
elucidated,
providing
more
alternative
therapeutic
targets
for
diseases
treatment.
Here,
we
provide
an
overview
basic
physiology
expound
regulatory
within
them.
We
also
address
crucial
role
pathogenesis
including
autoimmune,
neurodegenerative,
metabolic,
infectious
cancer,
with
a
focus
advances
macrophage‐targeted
strategies
exploring
modulation
components
regulators
pathways.
Last,
discuss
challenges
possible
solutions
therapy
clinical
applications.
hope
this
comprehensive
review
will
directions
further
research
targeting
macrophage
are
promising
to
improve
efficacy
International Journal of Biological Sciences,
Journal Year:
2024,
Volume and Issue:
20(3), P. 848 - 863
Published: Jan. 1, 2024
Macrophages
can
be
polarized
into
functional
classically
activated
(M1)
or
alternatively
(M2)
phenotype.
Tumor-associated
macrophages
(TAMs)
mainly
exhibit
M2
Previous
works
determined
that
up-regulation
of
enolase
2
(ENO2)
in
diffuse
large
B-cell
lymphoma
(DLBCL)
cells
promote
to
an
M2-like
phenotype,
thereby
consequently
promoting
the
progression
DLBCL.
Exosomes
are
a
subset
extracellular
vesicles,
carrying
various
bioactive
molecules,
mediate
signals
transduction
and
regulate
immune
cells.
In
our
study,
we
investigated
role
related
mechanisms
DLBCL-derived
exosomal
ENO2
regulating
macrophage
polarization
during
DLBCL
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(3), P. 1755 - 1755
Published: Feb. 1, 2024
This
article
provides
a
thorough
overview
of
the
biomarkers,
pathophysiology,
and
molecular
pathways
involved
in
transition
from
acute
kidney
injury
(AKI)
disease
(AKD)
to
chronic
(CKD).
It
categorizes
biomarkers
AKI
into
stress,
damage,
functional
markers,
highlighting
their
importance
early
detection,
prognosis,
clinical
applications.
review
also
highlights
links
between
renal
pathophysiological
mechanisms
underlying
AKD,
including
hypoperfusion,
sepsis,
nephrotoxicity,
immune
responses.
In
addition,
various
molecules
play
pivotal
roles
inflammation
hypoxia,
triggering
maladaptive
repair,
mitochondrial
dysfunction,
system
reactions,
cellular
senescence
cells.
Key
signaling
pathways,
such
as
Wnt/β-catenin,
TGF-β/SMAD,
Hippo/YAP/TAZ,
promote
fibrosis
impact
function.
The
renin-angiotensin-aldosterone
(RAAS)
triggers
cascade
leading
fibrosis,
with
aldosterone
exacerbating
oxidative
stress
changes
that
fibrosis.
evidence
suggests
RAS
inhibitors
may
protect
against
CKD
progression,
especially
post-AKI,
though
more
extensive
trials
are
needed
confirm
full
impact.
Cell Communication and Signaling,
Journal Year:
2024,
Volume and Issue:
22(1)
Published: April 26, 2024
Wound
healing
is
a
tightly
regulated
process
that
ensures
tissue
repair
and
normal
function
following
injury.
It
modulated
by
activation
of
pathways
such
as
the
transforming
growth
factor-beta
(TGF-β),
Notch,
Wnt/β-catenin
signaling
pathways.
Dysregulation
this
causes
poor
wound
healing,
which
leads
to
fibrosis
ulcerative
wounds.
The
pathway
involved
in
all
phases
primarily
proliferative
phase
for
formation
granulation
tissue.
This
review
focuses
on
role
its
transcriptional
regulation
target
genes.
crosstalk
between
Wnt/β-catenin,
TGF-β
pathways,
well
deregulation
chronic
wounds
are
also
considered,
with
special
focus
diabetic
ulcers.
Lastly,
we
discuss
current
prospective
therapies
wounds,
primary
strategies
photobiomodulation