Cells,
Journal Year:
2021,
Volume and Issue:
10(5), P. 1044 - 1044
Published: April 28, 2021
High
mobility
group
box-1
protein
(HMGB1),
a
member
of
the
high
superfamily,
is
an
abundant
and
ubiquitously
expressed
nuclear
protein.
Intracellular
HMGB1
released
by
immune
necrotic
cells
secreted
activates
range
cells,
contributing
to
excessive
release
inflammatory
cytokines
promoting
processes
such
as
cell
migration
adhesion.
Moreover,
typical
damage-associated
molecular
pattern
molecule
that
participates
in
various
responses.
In
these
ways,
it
plays
critical
role
pathophysiology
diseases.
Herein,
we
review
effects
on
types
describe
mechanisms
which
contributes
development
disorders.
Finally,
address
therapeutic
potential
targeting
HMGB1.
Frontiers in Immunology,
Journal Year:
2022,
Volume and Issue:
13
Published: April 26, 2022
Alzheimer's
disease
(AD)
is
the
most
prevalent
neurodegenerative
worldwide,
characterized
by
progressive
neuron
degeneration
or
loss
due
to
excessive
accumulation
of
β-amyloid
(Aβ)
peptides,
formation
neurofibrillary
tangles
(NFTs),
and
hyperphosphorylated
tau.
The
treatment
AD
has
been
only
partially
successful
as
majority
pharmacotherapies
on
market
may
alleviate
some
symptoms.
In
occurrence
AD,
increasing
attention
paid
neurodegeneration,
while
resident
glial
cells,
like
microglia
are
also
observed.
Microglia,
a
kind
crucial
cells
associated
with
innate
immune
response,
functions
double-edge
sword
role
in
CNS.
They
exert
beneficial
detrimental
influence
adjacent
neurons
through
secretion
both
pro-inflammatory
cytokines
well
neurotrophic
factors.
addition,
their
endocytosis
debris
toxic
protein
Aβ
tau
ensures
homeostasis
neuronal
microenvironment.
this
review,
we
will
systematically
summarize
recent
research
regarding
roles
pathology
latest
microglia-associated
therapeutic
targets
mainly
including
genes,
anti-inflammatory
genes
phagocytosis
at
length,
which
contradictory
controversial
warrant
further
be
investigated.
Frontiers in Cellular Neuroscience,
Journal Year:
2024,
Volume and Issue:
18
Published: Feb. 28, 2024
Traumatic
brain
injury
(TBI)
is
one
of
the
most
common
pathological
conditions
impacting
central
nervous
system
(CNS).
A
neurological
deficit
associated
with
TBI
results
from
a
complex
pathogenetic
mechanisms
including
glutamate
excitotoxicity,
inflammation,
demyelination,
programmed
cell
death,
or
development
edema.
The
critical
components
contributing
to
CNS
response,
damage
control,
and
regeneration
after
are
glial
cells–in
reaction
tissue
damage,
their
activation,
hypertrophy,
proliferation
occur,
followed
by
formation
scar.
scar
creates
barrier
in
damaged
helps
protect
acute
phase
post-injury.
However,
this
process
prevents
complete
recovery
late/chronic
producing
permanent
scarring,
which
significantly
impacts
function.
Various
types
participate
formation,
but
mostly
attributed
reactive
astrocytes
microglia,
play
important
roles
several
pathologies.
Novel
technologies
whole-genome
transcriptomic
epigenomic
analyses,
unbiased
proteomics,
show
that
both
microglia
represent
groups
heterogenic
subpopulations
different
genomic
functional
characteristics,
responsible
for
role
neurodegeneration,
neuroprotection
regeneration.
Depending
on
representation
distinct
glia
subpopulations,
as
well
regenerative
processes
delayed
neurodegeneration
may
thus
differ
nearby
remote
areas
structures.
This
review
summarizes
process,
where
resultant
effect
severity-,
region-
time-dependent
determined
model
distance
explored
area
lesion
site.
Here,
we
also
discuss
findings
concerning
intercellular
signaling,
long-term
possibilities
novel
therapeutical
approaches.
We
believe
comprehensive
study
an
emphasis
cells,
involved
post-injury
processes,
be
helpful
further
research
decisive
factor
when
choosing
model.
Cell Communication and Signaling,
Journal Year:
2024,
Volume and Issue:
22(1)
Published: March 6, 2024
Abstract
Microglia/macrophages
are
major
contributors
to
neuroinflammation
in
the
central
nervous
system
(CNS)
injury
and
exhibit
either
pro-
or
anti-inflammatory
phenotypes
response
specific
microenvironmental
signals.
Our
latest
vivo
vitro
studies
demonstrated
that
curcumin-treated
olfactory
ensheathing
cells
(aOECs)
can
effectively
enhance
neural
survival
axonal
outgrowth,
transplantation
of
aOECs
improves
neurological
outcome
after
spinal
cord
(SCI).
The
therapeutic
effect
is
largely
attributed
aOEC
activity
through
modulation
microglial
polarization
from
M1
M2
phenotype.
However,
very
little
known
about
what
viable
molecules
actively
responsible
for
switch
underlying
mechanisms
polarization.
Herein,
we
show
Interleukin-4
(IL-4)
plays
a
leading
role
triggering
phenotype,
appreciably
decreasing
levels
markers
IL‑1β,
IL‑6,
tumour
necrosis
factor-alpha
(TNF-α)
inducible
nitric
oxide
synthase
(iNOS)
elevating
Arg-1,
TGF-β,
IL-10,
CD206.
Strikingly,
blockade
IL-4
signaling
by
siRNA
neutralizing
antibody
medium
reverses
transition
M2,
activated
microglia
stimulated
with
lacking
significantly
decreases
neuronal
neurite
outgrowth.
In
addition,
improved
function
deficits
SCI
rats.
More
importantly,
crosstalk
between
JAK1/STAT1/3/6-targeted
downstream
signals
NF-κB/SOCS1/3
predominantly
orchestrates
IL-4-modulated
event.
These
results
provide
new
insights
into
molecular
driving
M1-to-M2
shift
shed
light
on
therapies
Chemical Engineering Journal,
Journal Year:
2024,
Volume and Issue:
488, P. 150631 - 150631
Published: March 26, 2024
The
skeletal
system
is
essential
for
preserving
body
structure
and
facilitating
mobility;
however,
bone
diseases
frequently
result
in
significant
disabilities,
necessitating
the
investigation
into
biomaterials
restoration.
Nevertheless,
these
may
elicit
immune
reactions
that
obstruct
healing
process.
Macrophages
assume
a
pivotal
role
modulating
inflammation
sustaining
homeostasis
regeneration.
A
comprehensive
understanding
of
molecular
interactions
between
macrophages
imperative
development
sophisticated
designed
to
regulate
environment
promote
remodeling.
This
review
delves
generation,
polarization,
interaction
with
principal
cell
types
implicated
osteogenesis,
detailing
mechanisms
by
which
influence
repair
their
response
biomaterials.
Additionally,
it
discusses
strategies
precise
modulation
macrophage
functionality
via
intelligent
mechanisms,
outlines
challenges
constraints
designing
integrate
functions.
By
elucidating
challenges,
lays
groundwork
creation
advanced
endowed
smart
immunomodulatory
capabilities,
heralding
novel
approaches
treatment
defects
advancement
regeneration
therapies.
Neural Regeneration Research,
Journal Year:
2021,
Volume and Issue:
17(1), P. 194 - 194
Published: June 11, 2021
Mesenchymal
stem
cell
(MSC)
transplantation
is
a
promising
treatment
strategy
for
spinal
cord
injury,
but
immunological
rejection
and
possible
tumor
formation
limit
its
application.
The
therapeutic
effects
of
MSCs
mainly
depend
on
their
release
soluble
paracrine
factors.
Exosomes
are
essential
the
secretion
these
effectors.
Bone
marrow
mesenchymal
cell-derived
exosomes
(BMSC-EXOs)
can
be
substituted
BMSCs
in
transplantation.
However,
underlying
mechanisms
remain
unclear.
In
this
study,
rat
model
T10
injury
was
established
using
impact
method.
Then,
30
minutes
1
day
after
rats
were
administered
200
μL
via
tail
vein
(200
μg/mL;
approximately
×
106
BMSCs).
Treatment
with
BMSC-EXOs
greatly
reduced
neuronal
death,
improved
myelin
arrangement
loss,
increased
pericyte/endothelial
coverage
vascular
wall,
decreased
blood-spinal
barrier
leakage,
caspase
expression,
inhibited
interleukin-1β
release,
accelerated
locomotor
functional
recovery
injury.
culture
experiment,
pericytes
treated
interferon-γ
necrosis
factor-α.
Lipofectamine
3000
used
to
deliver
lipopolysaccharide
into
cells,
cells
co-incubated
adenosine
triphosphate
simulate
vitro.
Pre-treatment
8
hours
pericyte
pyroptosis
survival
rate.
These
findings
suggest
that
may
protect
by
inhibiting
improving
integrity,
thereby
promoting
neurons
extension
nerve
fibers,
ultimately
motor
function
All
protocols
conducted
approval
Animal
Ethics
Committee
Zhengzhou
University
March
16,
2019.
Pharmaceutics,
Journal Year:
2022,
Volume and Issue:
14(1), P. 152 - 152
Published: Jan. 8, 2022
Traumatic
brain
injury
(TBI)
is
one
of
the
leading
causes
morbidity
and
mortality.
Consequences
vary
from
mild
cognitive
impairment
to
death
and,
no
matter
severity
subsequent
sequelae,
it
represents
a
high
burden
for
affected
patients
health
care
system.
Brain
trauma
can
cause
neuronal
through
mechanical
forces
that
disrupt
cell
architecture,
other
secondary
consequences
mechanisms
such
as
inflammation,
oxidative
stress,
programmed
death,
most
importantly,
excitotoxicity.
This
review
aims
provide
comprehensive
understanding
many
classical
novel
pathways
implicated
in
tissue
damage
following
TBI.
We
summarize
preclinical
evidence
potential
therapeutic
interventions
describe
available
clinical
evaluation
drug
targets
vitamin
B12
ifenprodil,
among
others.
International Journal of Molecular Sciences,
Journal Year:
2021,
Volume and Issue:
22(15), P. 8296 - 8296
Published: Aug. 2, 2021
Melatonin
interacts
in
multiple
ways
with
microglia,
both
directly
and,
via
routes
of
crosstalk
astrocytes
and
neurons,
indirectly.
These
effects
melatonin
are
relevance
terms
antioxidative
protection,
not
only
concerning
free-radical
detoxification,
but
also
prevention
processes
that
cause,
promote,
or
propagate
oxidative
stress
neurodegeneration,
such
as
overexcitation,
toxicological
insults,
viral
bacterial
infections,
sterile
inflammation
different
grades.
The
immunological
interplay
the
CNS,
microglia
playing
a
central
role,
is
high
complexity
includes
signaling
toward
endothelial
cells
other
leukocytes
by
cytokines,
chemokines,
nitric
oxide,
eikosanoids.
interferes
these
steps.
In
addition
to
canonical
signal
transduction
MT1
MT2
receptors,
secondary
tertiary
has
be
considered,
e.g.,
upregulation
sirtuins
modulation
pro-
anti-inflammatory
microRNAs.
Many
details
macrophage
functionality
obviously
applicable
microglial
cells.
Of
particular
interest
polarization
M2
subtypes
instead
M1,
i.e.,
favor
being
at
expense
proinflammatory
activities,
which
well-documented
macrophages
applies
microglia.
