Frontiers in Immunology,
Journal Year:
2019,
Volume and Issue:
10
Published: July 4, 2019
Historically,
systemic
self-inflammatory
conditions
were
classified
as
either
autoinflammatory
and
caused
by
the
innate
immune
system
or
autoimmune
driven
adaptive
responses.
However,
it
became
clear
that
reality
is
much
more
complex
autoimmune/inflammatory
range
along
an
"inflammatory
spectrum"
with
primarily
vs.
resembling
extremes
at
end.
Epigenetic
modifications
influence
gene
expression
alter
cellular
functions
without
modifying
genomic
sequence.
Methylation
of
CpG
DNA
dinucleotides
and/or
their
hydroxymethylation,
post-translational
to
amino
termini
histone
proteins,
non-coding
RNA
are
main
epigenetic
events.
The
pathophysiology
diseases
has
been
closely
linked
disease
causing
mutations
(rare)
a
combination
genetic
susceptibility
arising
from
exposure
environment
(more
common).
Over
recent
years,
progress
made
in
understanding
molecular
mechanisms
involved
inflammation
contribution
events
have
identified
i)
central
pathophysiological
factors
addition
predisposition
ii)
co-factors
determining
clinical
pictures
outcomes
individuals
mono-genic
disease.
Thus,
complete
contributors
will
result
approaches
predict
individual
introduction
effective,
target-directed
tolerable
therapies.
Here,
we
summarize
findings
signify
importance
disorders
inflammatory
spectrum
choosing
three
examples:
bone
condition
chronic
nonbacterial
osteomyelitis
(CNO),
"mixed
pattern"
disorder
psoriasis,
lupus
erythematosus
(SLE).
Cold Spring Harbor Perspectives in Biology,
Journal Year:
2016,
Volume and Issue:
8(9), P. a019505 - a019505
Published: May 18, 2016
Stephen
B.
Baylin1
and
Peter
A.
Jones2
1Cancer
Biology
Program,
Johns
Hopkins
University,
School
of
Medicine,
Baltimore,
Maryland
21287
2Van
Andel
Research
Institute,
Grand
Rapids,
Michigan
49503
Correspondence:
sbaylin{at}jhmi.edu
Cold Spring Harbor Perspectives in Medicine,
Journal Year:
2016,
Volume and Issue:
6(10), P. a026831 - a026831
Published: Sept. 6, 2016
Yixuan
Li
and
Edward
Seto
George
Washington
University
Cancer
Center,
Department
of
Biochemistry
Molecular
Medicine,
University,
Washington,
DC
20037
Correspondence:
seto{at}gwu.edu
Signal Transduction and Targeted Therapy,
Journal Year:
2019,
Volume and Issue:
4(1)
Published: Dec. 17, 2019
Epigenetic
alternations
concern
heritable
yet
reversible
changes
in
histone
or
DNA
modifications
that
regulate
gene
activity
beyond
the
underlying
sequence.
dysregulation
is
often
linked
to
human
disease,
notably
cancer.
With
development
of
various
drugs
targeting
epigenetic
regulators,
epigenetic-targeted
therapy
has
been
applied
treatment
hematological
malignancies
and
exhibited
viable
therapeutic
potential
for
solid
tumors
preclinical
clinical
trials.
In
this
review,
we
summarize
aberrant
functions
enzymes
methylation,
acetylation
methylation
during
tumor
progression
highlight
inhibitors
targeted
at
enzymes.
Cold Spring Harbor Perspectives in Biology,
Journal Year:
2016,
Volume and Issue:
8(4), P. a019521 - a019521
Published: April 1, 2016
Histone
posttranslational
modifications
represent
a
versatile
set
of
epigenetic
marks
involved
not
only
in
dynamic
cellular
processes,
such
as
transcription
and
DNA
repair,
but
also
the
stable
maintenance
repressive
chromatin.
In
this
article,
we
review
many
key
newly
identified
histone
known
to
be
deregulated
cancer
how
impacts
function.
The
latter
part
article
addresses
challenges
current
status
drug
development
process
it
applies
therapeutics.
Cardiovascular Research,
Journal Year:
2020,
Volume and Issue:
117(6), P. 1450 - 1488
Published: Oct. 26, 2020
Abstract
Myocardial
fibrosis,
the
expansion
of
cardiac
interstitium
through
deposition
extracellular
matrix
proteins,
is
a
common
pathophysiologic
companion
many
different
myocardial
conditions.
Fibrosis
may
reflect
activation
reparative
or
maladaptive
processes.
Activated
fibroblasts
and
myofibroblasts
are
central
cellular
effectors
in
serving
as
main
source
proteins.
Immune
cells,
vascular
cells
cardiomyocytes
also
acquire
fibrogenic
phenotype
under
conditions
stress,
activating
fibroblast
populations.
Fibrogenic
growth
factors
(such
transforming
factor-β
platelet-derived
factors),
cytokines
[including
tumour
necrosis
factor-α,
interleukin
(IL)-1,
IL-6,
IL-10,
IL-4],
neurohumoral
pathways
trigger
signalling
cascades
binding
to
surface
receptors,
downstream
cascades.
In
addition,
matricellular
macromolecules
deposited
remodelling
myocardium
regulate
assembly,
while
modulating
signal
transduction
protease
factor
activity.
Cardiac
can
sense
mechanical
stress
mechanosensitive
ion
channels
integrins,
intracellular
that
contribute
fibrosis
response
pressure
overload.
Although
subpopulations
fibroblast-like
exert
important
protective
actions
both
interstitial/perivascular
ultimately
fibrotic
changes
perturb
systolic
diastolic
function,
play
an
role
pathogenesis
arrhythmias.
This
review
article
discusses
molecular
mechanisms
involved
various
diseases,
including
infarction,
heart
failure
with
reduced
preserved
ejection
fraction,
genetic
cardiomyopathies,
diabetic
disease.
Development
fibrosis-targeting
therapies
for
patients
diseases
will
require
not
only
understanding
functional
pluralism
dissection
basis
remodelling,
but
appreciation
heterogeneity
fibrosis-associated
Cold Spring Harbor Perspectives in Biology,
Journal Year:
2014,
Volume and Issue:
6(7), P. a018762 - a018762
Published: July 1, 2014
Ronen
Marmorstein1
and
Ming-Ming
Zhou2
1Program
in
Gene
Expression
Regulation,
Wistar
Institute,
Department
of
Chemistry,
University
Pennsylvania,
Philadelphia,
19104
2Department
Structural
Chemical
Biology,
Icahn
School
Medicine
at
Mount
Sinai,
New
York,
York
10065
Correspondence:
marmor{at}wistar.org
