Frontiers in Immunology,
Journal Year:
2023,
Volume and Issue:
14
Published: Jan. 26, 2023
Responding
to
tissue
injury,
skeletal
muscles
undergo
the
destruction
and
reconstruction
accompanied
with
inflammation.
The
immune
system
recognizes
molecules
released
from
or
exposed
on
damaged
tissue.
In
local
minor
damage,
tissue-resident
macrophages
sequester
pro-inflammatory
debris
prevent
initiation
of
most
cases
muscle
however,
a
cascade
inflammation
will
be
initiated
through
activation
mast
cells
recruitment
blood
circulation
injured
site
by
recongnization
damage-associated
molecular
patterns
(DAMPs)
activated
complement
system.
During
inflammation,
neutrophils
scavenge
release
inflammatory
cytokines
latter
stimulates
myoblast
fusion
vascularization
promote
repair.
On
other
hand,
an
abundance
chemokines
causes
profound
hyper-inflammation
mobilization
trigger
vicious
cycle
lead
cytokine
storm.
storm
results
in
elevation
cytolytic
cytotoxic
reactive
oxygen
species
(ROS)
aggravates
including
healthy
bystander
Severe
can
rhabdomyolysis
cause
sepsis-like
systemic
response
syndrome
(SIRS)
remote
organ
damage.
Therefore,
understanding
more
details
involvement
factors
damage
repair
provide
new
precise
therapeutic
strategies,
attenuation
promotion
Frontiers in Immunology,
Journal Year:
2021,
Volume and Issue:
12
Published: Aug. 12, 2021
Macrophages
are
dynamic
cells
that
play
critical
roles
in
the
induction
and
resolution
of
sterile
inflammation.
In
this
review,
we
will
compile
interpret
recent
findings
on
plasticity
macrophages
how
these
contribute
to
development
non-infectious
inflammatory
diseases,
with
a
particular
focus
allergic
autoimmune
disorders.
The
inflammation
then
be
examined,
emphasizing
ability
clear
apoptotic
immune
cells.
Rheumatoid
arthritis
(RA)
is
chronic
autoimmune-driven
spectrum
diseases
where
persistent
results
synovial
hyperplasia
excessive
cell
accumulation,
leading
remodeling
reduced
function
affected
joints.
central
pathophysiology
RA,
driving
episodic
cycles
tissue
destruction.
RA
patients
have
increased
numbers
active
M1
polarized
pro-inflammatory
few
or
inactive
M2
type
This
imbalance
macrophage
homeostasis
main
contributor
mediators
resulting
continual
activation
stromal
populations
accelerated
remodeling.
Modulation
phenotype
remains
key
therapeutic
goal
for
treatment
disease.
Intriguingly,
intervention
glucocorticoids
other
DMARDs
promotes
re-polarization
an
anti-inflammatory
phenotype;
reprogramming
dependent
metabolic
changes
promote
phenotypic
switching.
Allergic
asthma
associated
Th2-polarised
airway
inflammation,
structural
large
airways,
hyperresponsiveness.
Macrophage
polarization
has
profound
impact
pathogenesis,
as
response
allergen
exposure
regulated
by
intricate
interplay
between
local
factors
including
cytokines,
chemokines
danger
signals
from
neighboring
Th2-polarized
environment
characteristic
asthma,
high
levels
IL-4
produced
locally
infiltrating
innate
lymphoid
helper
T
acquisition
alternatively
activated
M2a
macrophages,
myriad
effects
structure.
Targeting
regulators
currently
being
pursued
diseases.
re-balancing
responses
towards
pro-resolution
thus
success
response.
It
long
been
established
apoptosis
supports
monocyte
recruitment
sites
facilitating
subsequent
corpse
clearance.
drives
mediates
switch
polarity
macrophages.
However,
role
cell-derived
extracellular
vesicles
(ACdEV)
control
received
remarkably
little
attention.
ACdEV
powerful
intercellular
communication,
carrying
wealth
lipid
protein
may
modulate
phenotype,
cargo
immune-modulating
enzymes.
such
interactions
result
repair
disease
different
contexts.
discuss
origin,
characterization,
activity
underlying
mechanisms
via
clearance,
order
provide
new
insights
into
strategies
could
exploit
capabilities
agile
responsive
Frontiers in Immunology,
Journal Year:
2019,
Volume and Issue:
10
Published: Dec. 3, 2019
Hepatic
macrophages
play
a
central
role
in
maintaining
homeostasis
the
liver,
as
well
initiation
and
progression
of
liver
diseases.
can
mainly
derive
from
resident
hepatic
called
Kupffer
cells
or
circulating
bone
marrow-derived
monocytes.
are
self-renewing
typically
non-migrating
stationed
sinusoids
contrast
to
originating
regulate
by
mediating
immunity
against
non-pathogenic
blood-borne
molecules,
while
participating
coordinated
immune
responses
leading
pathogen
clearance,
leukocyte
recruitment
antigen
presentation
lymphocytes
present
vasculature.
Monocyte-derived
infiltrate
into
tissue
when
metabolic
toxic
damage
instigates
likely
dispensable
for
replenishing
macrophage
population
homeostasis.
In
recent
years,
different
populations
have
been
identified
with
distinct
phenotypes
discrete
functions,
far
beyond
dogma
M1
M2
macrophages.
pathogenesis
acute
chronic
failure,
fibrosis,
non-alcoholic
fatty
disease,
alcoholic
viral
hepatitis,
hepatocellular
carcinoma,
disease
resolution.
The
understanding
diseases
provides
opportunities
development
targeted
therapeutics
respective
malignancies.
This
review
will
summarize
current
knowledge
macrophages,
their
origin,
critical
resolution
Furthermore,
we
provide
comprehensive
overview
therapeutic
targeting
strategies
developed
treatment
International Journal of Molecular Sciences,
Journal Year:
2020,
Volume and Issue:
21(3), P. 1105 - 1105
Published: Feb. 7, 2020
Cutaneous
fibrosis
results
from
suboptimal
wound
healing
following
significant
tissue
injury
such
as
severe
burns,
trauma,
and
major
surgeries.
Pathologic
skin
in
scars
that
are
disfiguring,
limit
normal
movement,
prevent
patient
recovery
reintegration
into
society.
While
various
therapeutic
strategies
have
been
used
to
accelerate
decrease
the
incidence
of
scarring,
recent
studies
targeted
molecular
regulators
each
phase
healing,
including
inflammatory,
proliferative,
remodeling
phases.
Here,
we
reviewed
most
literature
elucidating
pathways
can
be
reduce
with
a
particular
focus
on
post-burn
scarring.
Current
research
targeting
inflammatory
mediators,
epithelial
mesenchymal
transition,
myofibroblast
differentiation
shows
promising
results.
However,
multimodal
approach
addressing
all
three
phases
may
provide
best
outcome.