Experimental Biology and Medicine,
Год журнала:
2024,
Номер
249
Опубликована: Фев. 28, 2024
Neuroinflammation
is
considered
a
balanced
inflammatory
response
important
in
the
intrinsic
repair
process
after
injury
or
infection.
Under
chronic
states
of
disease,
injury,
infection,
persistent
neuroinflammation
results
heightened
presence
cytokines,
chemokines,
and
reactive
oxygen
species
that
result
tissue
damage.
In
CNS,
surrounding
microglia
normally
contain
macrophages
other
innate
immune
cells
perform
active
surveillance.
The
resulting
cytokines
produced
by
these
affect
growth,
development,
responsiveness
present
both
white
gray
matter
regions
CNS.
Controlling
levels
ultimately
improves
neurocognitive
function
lesions
associated
with
neurologic
disease.
MicroRNAs
(miRNAs)
are
master
regulators
genome
subsequently
control
activity
responses
crucial
sustaining
robust
acute
immunological
towards
an
infection
while
dampening
pathways
chemokines
neuroinflammation.
Numerous
reports
have
directly
implicated
miRNAs
controlling
abundance
interleukins,
TGF-B,
NF-kB,
toll-like
receptor-signaling
intrinsically
linked
development
neurological
disorders
such
as
Parkinson’s,
ALS,
epilepsy,
Alzheimer’s,
neuromuscular
degeneration.
This
review
focused
on
discussing
role
play
regulating
initiating
states,
many
which
maintain
level
and/or
neuron-specific
secondary
messengers.
Dysregulated
microglia,
astrocytes,
oligodendrocytes,
epididymal
cells,
contribute
to
overall
glial-specific
niche
impacts
neuronal
conductivity,
signaling
action
potentials,
neurotransmitter
robustness,
neuron-neuron
specific
communication,
neuron-muscular
connections.
Understanding
regulate
microglial
activation
step
forward
developing
non-coding
RNA-based
therapeutics
treat
potentially
correct
behavioral
cognitive
deficits
typically
found
patients
suffering
from
Cell Communication and Signaling,
Год журнала:
2023,
Номер
21(1)
Опубликована: Март 14, 2023
Doxorubicin
(DOX)
is
a
powerful
and
commonly
used
chemotherapeutic
drug,
alone
or
in
combination
variety
of
cancers,
while
it
has
been
found
to
cause
serious
cardiac
side
effects
clinical
application.
More
more
researchers
are
trying
explore
the
molecular
mechanisms
DOX-induced
cardiomyopathy
(DIC),
which
oxidative
stress
inflammation
considered
play
significant
role.
This
review
summarizes
signaling
pathways
related
DIC
compounds
that
exert
cardioprotective
by
acting
on
relevant
pathways,
including
role
Nrf2/Keap1/ARE,
Sirt1/p66Shc,
Sirt1/PPAR/PGC-1α
NOS,
NOX,
Fe2+
stress,
as
well
NLRP3/caspase-1/GSDMD,
HMGB1/TLR4/MAPKs/NF-κB,
mTOR/TFEB/NF-κB
inflammation.
Hence,
we
attempt
explain
terms
inflammation,
provide
theoretical
basis
new
idea
for
further
drug
research
reducing
DIC.
Video
Abstract.
Frontiers in Aging Neuroscience,
Год журнала:
2024,
Номер
16
Опубликована: Апрель 12, 2024
Neuroinflammation
refers
to
a
highly
complicated
reaction
of
the
central
nervous
system
(CNS)
certain
stimuli
such
as
trauma,
infection,
and
neurodegenerative
diseases.
This
is
cellular
immune
response
whereby
glial
cells
are
activated,
inflammatory
mediators
liberated
reactive
oxygen
nitrogen
species
synthesized.
key
process
that
helps
protect
brain
from
pathogens,
but
inappropriate,
or
protracted
inflammation
yields
pathological
states
Parkinson’s
disease,
Alzheimer’s,
Multiple
Sclerosis,
other
disorders
showcase
various
pathways
neurodegeneration
distributed
in
parts
CNS.
review
reveals
major
neuroinflammatory
signaling
associated
with
neurodegeneration.
Additionally,
it
explores
promising
therapeutic
avenues,
stem
cell
therapy,
genetic
intervention,
nanoparticles,
aiming
regulate
neuroinflammation
potentially
impede
decelerate
advancement
these
conditions.
A
comprehensive
understanding
intricate
connection
between
diseases
pivotal
for
development
future
treatment
strategies
can
alleviate
burden
imposed
by
devastating
disorders.
Microorganisms,
Год журнала:
2023,
Номер
11(9), С. 2169 - 2169
Опубликована: Авг. 28, 2023
Urinary
tract
infections
(UTIs)
are
among
the
most
common
bacterial
infections,
especially
women
and
older
adults,
leading
to
a
significant
global
healthcare
cost
burden.
Uropathogenic
Frontiers in Medicine,
Год журнала:
2023,
Номер
10
Опубликована: Ноя. 21, 2023
Sepsis
is
a
systemic
inflammatory
disease
caused
by
severe
infections
that
involves
multiple
organs,
among
which
the
lung
most
susceptible,
leaving
patients
highly
vulnerable
to
acute
injury
(ALI).
Refractory
hypoxemia
and
respiratory
distress
are
classic
clinical
symptoms
of
ALI
sepsis,
has
mortality
rate
40%.
Despite
extensive
research
on
mechanisms
exact
pathological
process
not
fully
understood.
This
article
reviews
advances
in
pathogenesis
sepsis
focusing
treatment
regimens
adopted
practice
for
corresponding
molecular
mechanisms.
review
can
only
contribute
theories
but
also
recommend
new
strategies
related
injuries.
Cells,
Год журнала:
2023,
Номер
12(10), С. 1351 - 1351
Опубликована: Май 9, 2023
The
development
of
antiretroviral
drugs
(ARVs)
was
a
great
milestone
in
the
management
HIV
infection.
ARVs
suppress
viral
activity
host
cell,
thus
minimizing
injury
to
cells
and
prolonging
life.
However,
an
effective
treatment
has
remained
elusive
for
four
decades
due
successful
immune
evasion
mechanisms
virus.
A
thorough
understanding
molecular
interaction
with
cell
is
essential
both
preventive
curative
therapies
This
review
highlights
several
inherent
that
promote
its
survival
propagation,
such
as
targeting
CD4+
lymphocytes,
downregulation
MHC
class
I
II,
antigenic
variation
envelope
complex
minimizes
antibody
access,
how
they
collaboratively
render
system
unable
mount
response.
International Journal of Molecular Sciences,
Год журнала:
2023,
Номер
24(12), С. 9818 - 9818
Опубликована: Июнь 6, 2023
The
comprehensive
anabolic
effects
of
insulin
throughout
the
body,
in
addition
to
control
glycemia,
include
ensuring
lipid
homeostasis
and
anti-inflammatory
modulation,
especially
adipose
tissue
(AT).
prevalence
obesity,
defined
as
a
body
mass
index
(BMI)
≥
30
kg/m2,
has
been
increasing
worldwide
on
pandemic
scale
with
accompanying
syndemic
health
problems,
including
glucose
intolerance,
resistance
(IR),
diabetes.
Impaired
sensitivity
or
IR
paradoxically
leads
diseases
an
inflammatory
component
despite
hyperinsulinemia.
Therefore,
excess
visceral
AT
obesity
initiates
chronic
low-grade
conditions
that
interfere
signaling
via
receptors
(INSRs).
Moreover,
response
IR,
hyperglycemia
itself
stimulates
primarily
defensive
associated
subsequent
release
numerous
cytokines
real
threat
organ
function
deterioration.
In
this
review,
all
components
vicious
cycle
are
characterized
particular
emphasis
interplay
between
both
innate
adaptive
immune
responses
related
obesity.
Increased
accumulation
should
be
considered
main
environmental
factor
responsible
for
disruption
epigenetic
regulatory
mechanisms
system,
resulting
autoimmunity
inflammation.
Abstract
Macrophages
are
versatile
immune
cells
with
remarkable
plasticity,
enabling
them
to
adapt
diverse
tissue
microenvironments
and
perform
various
functions.
Traditionally
categorized
into
classically
activated
(M1)
alternatively
(M2)
phenotypes,
recent
advances
have
revealed
a
spectrum
of
macrophage
activation
states
that
extend
beyond
this
dichotomy.
The
complex
interplay
signaling
pathways,
transcriptional
regulators,
epigenetic
modifications
orchestrates
polarization,
allowing
respond
stimuli
dynamically.
Here,
we
provide
comprehensive
overview
the
cascades
governing
focusing
on
roles
Toll‐like
receptors,
signal
transducer
activator
transcription
proteins,
nuclear
microRNAs.
We
also
discuss
emerging
concepts
metabolic
reprogramming
trained
immunity,
contributing
their
functional
adaptability.
Macrophage
plasticity
plays
pivotal
role
in
repair
regeneration,
macrophages
coordinating
inflammation,
angiogenesis,
matrix
remodeling
restore
homeostasis.
By
harnessing
potential
novel
therapeutic
strategies
targeting
polarization
could
be
developed
for
diseases,
including
chronic
wounds,
fibrotic
disorders,
inflammatory
conditions.
Ultimately,
deeper
understanding
molecular
mechanisms
underpinning
will
pave
way
innovative
regenerative
medicine
engineering
approaches.
In
mammals,
males
and
females
show
marked
differences
in
immune
responses.
Males
are
globally
more
sensitive
to
infectious
diseases,
while
susceptible
systemic
autoimmunity.
X-chromosome
inactivation
(XCI),
the
epigenetic
mechanism
ensuring
silencing
of
one
X
females,
may
participate
these
sex
biases.
We
perturbed
expression
trigger
XCI,
noncoding
RNA
Xist
,
female
mice.
This
resulted
reactivation
genes
on
inactive
X,
including
members
Toll-like
receptor
7
(TLR7)
signaling
pathway,
monocyte/macrophages
dendritic
B
cells.
Consequently,
mice
spontaneously
developed
inflammatory
signs
typical
lupus,
anti–nucleic
acid
autoantibodies,
increased
frequencies
age-associated
germinal
center
cells,
expansion
Mechanistically,
TLR7
is
dysregulated
macrophages,
leading
sustained
target
upon
stimulation.
These
findings
provide
a
direct
link
between
maintenance
XCI
female-biased
autoimmune
manifestations
highlight
altered
as
cause