Genes,
Год журнала:
2023,
Номер
14(3), С. 555 - 555
Опубликована: Фев. 23, 2023
Immune
Thrombocytopenia
(ITP)
is
an
autoimmune
blood
disorder
that
involves
multiple
pathways
responsible
for
the
homeostasis
of
immune
system.
Numerous
pieces
literature
have
proposed
potential
immune-related
genes
as
diagnostic
and
prognostic
biomarkers,
which
mostly
implicate
role
B
cells
T
in
pathogenesis
ITP.
However,
a
more
in-depth
understanding
required
how
these
are
regulated.
Thus,
this
scoping
review
aims
to
collate
evidence
further
elucidate
each
possible
epigenetics
mechanism
regulation
immunological
pertinent
This
encompasses
DNA
methylation,
histone
modification,
non-coding
RNA.
A
total
41
studies
were
scrutinized
clarify
mechanisms
related
Identifying
will
provide
new
paradigm
may
assist
diagnosis
treatment
thrombocytopenia.
Biomolecules,
Год журнала:
2020,
Номер
10(7), С. 1044 - 1044
Опубликована: Июль 14, 2020
Immune
responses
are
essential
for
the
clearance
of
pathogens
and
repair
injured
tissues;
however,
if
these
not
properly
controlled,
autoimmune
diseases
can
occur.
Autoimmune
(ADs)
a
family
disorders
characterized
by
body's
immune
response
being
directed
against
its
own
tissues,
with
consequent
chronic
inflammation
tissue
damage.
Despite
enormous
efforts
to
identify
new
drug
targets
develop
therapies
prevent
ameliorate
AD
symptoms,
no
definitive
solutions
available
today.
Additionally,
while
substantial
progress
has
been
made
in
development
some
ADs,
most
treatments
only
symptoms
and,
general,
ADs
still
incurable.
Hundreds
genetic
loci
have
identified
associated
genome-wide
association
studies.
However,
whole
list
molecular
factors
that
contribute
pathogenesis
is
unknown.
Noncoding
(nc)RNAs,
such
as
microRNAs,
circular
(circ)RNAs,
long
noncoding
(lnc)RNAs,
regulate
gene
expression
at
different
levels
various
diseases,
including
serve
potential
well
biomarkers
disease
progression
therapy.
In
this
review,
we
will
focus
on
roles
regulation
ncRNA
four
diseases-systemic
lupus
erythematosus,
rheumatoid
arthritis,
multiple
sclerosis,
type
1
diabetes
mellitus.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(5), С. 2750 - 2750
Опубликована: Фев. 27, 2024
Inflammation
is
a
key
contributor
to
both
the
initiation
and
progression
of
tumors,
it
can
be
triggered
by
genetic
instability
within
as
well
lifestyle
dietary
factors.
The
inflammatory
response
plays
critical
role
in
epigenetic
reprogramming
tumor
cells,
cells
that
comprise
microenvironment.
Cells
microenvironment
acquire
phenotype
promotes
immune
evasion,
progression,
metastasis.
We
will
review
mechanisms
pathways
involved
interaction
between
inflammation,
nutrition,
limitations
current
therapies,
discuss
potential
future
therapeutic
approaches.
Frontiers in Immunology,
Год журнала:
2021,
Номер
12
Опубликована: Дек. 23, 2021
Systemic
lupus
erythematosus
(SLE)
and
rheumatoid
arthritis
(RA)
are
two
common
multisystem
autoimmune
diseases
that
share,
among
others,
many
clinical
manifestations
serological
features.
The
role
of
long
non-coding
RNAs
(lncRNAs)
has
been
particular
interest
in
the
pathogenesis
diseases.
Here,
we
aimed
to
summarize
roles
lncRNAs
as
emerging
novel
biomarkers
therapeutic
targets
SLE
RA.
We
conducted
a
narrative
review
summarizing
original
articles
on
associated
with
RA,
published
until
November
1,
2021.
Based
studies
lncRNA
expression
profiles
samples
(including
PBMCs,
serum,
exosomes),
it
was
noted
most
current
research
is
focused
investigating
regulatory
mechanisms
these
and/or
Several
have
hypothesized
play
key
In
SLE,
such
GAS5,
NEAT1,
TUG1,
linc0949,
linc0597
dysregulated
may
serve
targets.
validated
lncRNAs,
HOTAIR,
HIX003209,
identified
promising
for
both
diagnosis
treatment.
shared
example,
participate
through
mitogen-activated
protein
kinase
pathway
trigger
AMP-activated
data
drive
RA
could
potentially
coming
future.
Frontiers in Pharmacology,
Год журнала:
2021,
Номер
12
Опубликована: Март 12, 2021
Rheumatoid
arthritis
(RA)
is
a
chronic
autoimmune
disease
of
unknown
etiology,
mainly
manifested
by
persistent
abnormal
proliferation
fibroblast-like
synoviocytes
(FLSs),
inflammation,
synovial
hyperplasia
and
cartilage
erosion,
accompanied
joint
swelling
destruction.
Abnormal
expression
or
function
long
noncoding
RNAs
(lncRNAs)
are
closely
related
to
human
diseases,
including
cancers,
mental
diseases
others.
The
sequence
spatial
structure
lncRNAs,
the
disorder
interaction
with
binding
protein
will
lead
change
gene
in
way
epigenetic
modification.
Increasing
evidence
demonstrated
that
lncRNAs
were
involved
activation
FLSs,
which
played
key
role
pathogenesis
RA.
In
this
review,
research
progress
RA
was
systematically
summarized,
diagnosis
RA,
regulatory
mechanism
intervention
treatment
Furthermore,
activated
signal
pathways,
DNA
methylation
other
have
also
been
overview
review.
Journal of Neuroinflammation,
Год журнала:
2021,
Номер
18(1)
Опубликована: Янв. 6, 2021
Abstract
Background
Microglia
are
resident
immunocompetent
and
phagocytic
cells
in
the
CNS.
Pro-inflammatory
microglia,
stimulated
by
microbial
signals
such
as
bacterial
lipopolysaccharide
(LPS),
viral
RNAs,
or
inflammatory
cytokines,
neurotoxic
associated
with
pathogenesis
of
several
neurodegenerative
diseases.
Long
non-coding
RNAs
(lncRNA)
emerging
important
tissue-specific
regulatory
molecules
directing
cell
differentiation
functional
states
may
help
direct
proinflammatory
responses
microglia.
Characterization
lncRNAs
upregulated
NR_126553
2500002B13Rik,
now
termed
Nostrill
(iNOS
Transcriptional
Regulatory
Intergenic
LncRNA
Locus)
increases
our
understanding
molecular
mechanisms
CNS
innate
immunity.
Methods
Microglial
gene
expression
array
analyses
qRT-PCR
were
used
to
identify
a
novel
long
intergenic
RNA,
Nostrill,
LPS-stimulated
microglial
lines,
primary
LPS-injected
mouse
cortical
tissue.
Silencing
overexpression
studies,
RNA
immunoprecipitation,
chromatin
isolation
purification
assays,
study
function
this
In
vitro
assays
examine
effects
silencing
microglia
on
neurotoxicity.
Results
We
report
here
characterization
lncRNA,
NR_126553,
2500002B13Rik
Locus).
is
induced
LPS
stimulation
BV2
cells,
murine
tissue
mice.
Induction
NF-κB
dependent
decreased
inducible
nitric
oxide
synthase
(iNOS)
(NO)
production
cells.
Overexpression
increased
iNOS
NO
production.
immunoprecipitation
demonstrated
that
physically
subunit
p65
following
stimulation.
significantly
reduced
polymerase
II
recruitment
promoter
H3K4me3
activating
histone
modifications
at
loci.
studies
Conclusions
Our
data
indicate
new
role
NF-κB-induced
suggest
acts
co-activator
transcription
resulting
through
modulation
epigenetic
remodeling.
be
target
for
reducing
neurotoxicity
iNOS-mediated
processes
during
neurodegeneration.
