Biochemical Society Transactions,
Journal Year:
2022,
Volume and Issue:
50(5), P. 1341 - 1352
Published: Oct. 25, 2022
Extracellular
signal-related
kinases
1
and
2
(ERK1/2)
are
the
final
components
of
mitogen-activated
protein
kinase
(MAPK)
phosphorylation
cascade,
an
integral
module
in
a
diverse
array
signalling
pathways
for
shaping
cell
behaviour
fate.
More
recently,
studies
have
shown
that
ERK1/2
plays
essential
role
downstream
immune
receptors
to
elicit
inflammatory
gene
expression
response
infection
or
tissue
damage.
Much
this
work
has
studied
activation
Toll-like
receptor
(TLR)
pathways,
providing
mechanistic
insights
into
its
recruitment,
compartmentalisation
cells
innate
system.
In
review,
we
summarise
typical
growth
factor
before
discussing
known
roles
with
focus
TLRs.
We
examine
emerging
research
uncovering
evidence
dysfunctional
diseases
discuss
potential
therapeutic
benefit
targeting
inflammation.
Cell Death and Disease,
Journal Year:
2023,
Volume and Issue:
14(3)
Published: March 21, 2023
Abstract
Ferroptosis
is
an
iron-dependent
regulated
cell
death
driven
by
excessive
lipid
peroxidation.
Inflammation
one
common
and
effective
physiological
event
that
protects
against
various
stimuli
to
maintain
tissue
homeostasis.
However,
the
dysregulation
of
inflammatory
responses
can
cause
imbalance
immune
system,
dysfunction
death.
Recent
studies
have
pointed
out
activation
inflammation,
including
multiple
inflammation-related
signaling
pathways,
lead
ferroptosis.
Among
related
signal
transduction
we
focused
on
five
classical
namely,
JAK-STAT,
NF-κB,
inflammasome,
cGAS-STING
MAPK
expounded
their
roles
in
To
date,
many
agents
shown
therapeutic
effects
ferroptosis-related
diseases
modulating
aforementioned
pathways
vivo
vitro.
Moreover,
regulatory
these
iron
metabolism
peroxidation
been
described
detail,
contributing
further
understanding
pathophysiological
process
Taken
together,
targeting
inflammation
will
provide
appropriate
ways
intervene
ferroptosis
diseases.
Journal of Hematology & Oncology,
Journal Year:
2023,
Volume and Issue:
16(1)
Published: Nov. 30, 2023
Inflammation
is
a
fundamental
defensive
response
to
harmful
stimuli,
but
the
overactivation
of
inflammatory
responses
associated
with
most
human
diseases.
Reactive
oxygen
species
(ROS)
are
class
chemicals
that
generated
after
incomplete
reduction
molecular
oxygen.
At
moderate
levels,
ROS
function
as
critical
signaling
molecules
in
modulation
various
physiological
functions,
including
responses.
However,
at
excessive
exert
toxic
effects
and
directly
oxidize
biological
macromolecules,
such
proteins,
nucleic
acids
lipids,
further
exacerbating
development
causing
Therefore,
designing
manufacturing
biomaterials
scavenge
has
emerged
an
important
approach
for
restoring
homeostasis,
limiting
protecting
host
against
damage.
This
review
systematically
outlines
dynamic
balance
production
clearance
under
conditions.
We
focus
on
mechanisms
by
which
regulate
cell
proteins
how
these
affect
inflammation.
Furthermore,
we
discuss
use
potential
currently
available-biomaterials
ROS,
agents
were
engineered
reduce
levels
blocking
generation,
chemically
reacting
or
catalytically
accelerating
clearance,
treatment
Finally,
evaluate
challenges
prospects
controlled
material
design
scavenging
biomaterials.
Antioxidants,
Journal Year:
2022,
Volume and Issue:
11(12), P. 2377 - 2377
Published: Nov. 30, 2022
Cerebral
ischemic
stroke
is
characterized
by
acute
ischemia
in
a
certain
part
of
the
brain,
which
leads
to
brain
cells
necrosis,
apoptosis,
ferroptosis,
pyroptosis,
etc.
At
present,
there
are
limited
effective
clinical
treatments
for
cerebral
stroke,
and
recovery
blood
circulation
will
lead
ischemia-reperfusion
injury
(CIRI).
involves
many
pathological
processes
such
as
oxidative
stress,
inflammation,
mitochondrial
dysfunction.
Nuclear
factor
erythroid
2-related
2
(Nrf2),
one
most
critical
antioxidant
transcription
factors
cells,
can
coordinate
various
cytoprotective
inhibit
stress.
Targeting
Nrf2
considered
potential
strategy
prevent
treat
injury.
During
ischemia,
participates
signaling
pathways
Keap1,
PI3K/AKT,
MAPK,
NF-κB,
HO-1,
then
alleviates
or
CIRI
inhibiting
anti-inflammation,
maintaining
homeostasis,
protecting
blood–brain
barrier,
ferroptosis.
In
this
review,
we
have
discussed
structure
Nrf2,
mechanisms
related
research
on
treatment
through
pathway
recent
years,
expounded
important
role
future
stroke.
Cell Stress and Chaperones,
Journal Year:
2017,
Volume and Issue:
23(1), P. 101 - 113
Published: July 1, 2017
The
cardiac
microvascular
reperfusion
injury
is
characterized
by
the
endothelial
cells
(CMECs)
oxidative
damage
which
responsible
for
progression
of
dysfunction.
However,
few
strategies
are
available
to
reverse
such
pathologies.
This
study
aimed
explore
mechanism
stress
induced
CMECs
death
and
beneficial
actions
melatonin
on
survival,
with
a
special
focused
IP3R-[Ca2+]c/VDAC-[Ca2+]m
axis
MAPK/ERK
survival
signaling.
We
found
that
H2O2
significantly
activated
cAMP
response
element
binding
protein
(CREB)
enhanced
IP3R
VDAC
transcription
expression,
leading
[Ca2+]c
[Ca2+]m
overload.
High
concentration
suppressed
ΔΨm,
opened
mPTP,
released
cyt-c
into
cytoplasm
where
it
mitochondria-dependent
pathway.
could
protect
against
via
stimulation
inactivated
CREB
therefore
blocked
IP3R/VDAC
upregulation
[Ca2+]c/[Ca2+]m
overload,
sustaining
mitochondrial
structural
function
integrity
ultimately
blockading
mitochondrial-mediated
cellular
death.
In
summary,
these
findings
confirmed
mechanisms
mitochondrial-involved
provided
an
attractive
effective
way
enhance
survival.
Frontiers in Immunology,
Journal Year:
2021,
Volume and Issue:
12
Published: Dec. 7, 2021
Periodontitis
(PD)
is
a
common
chronic
infectious
disease.
The
local
inflammatory
response
in
the
host
may
cause
destruction
of
supporting
periodontal
tissue.
Macrophages
play
variety
roles
PD,
including
regulatory
and
phagocytosis.
Moreover,
under
induction
different
factors,
macrophages
polarize
form
functional
phenotypes.
Among
them,
M1-type
with
proinflammatory
functions
M2-type
anti-inflammatory
are
most
representative,
both
them
can
regulate
tendency
immune
system
to
exert
or
functions.
M1
M2
involved
destructive
reparative
stages
PD.
Due
complex
microenvironment
dynamic
development
various
mediators,
increasing
attention
has
been
given
study
macrophage
polarization
This
review
summarizes
role
PD
its
research
progress.
International Journal of Molecular Sciences,
Journal Year:
2019,
Volume and Issue:
20(6), P. 1483 - 1483
Published: March 25, 2019
The
discovery
of
the
role
RAS/RAF/MEK/ERK
pathway
in
melanomagenesis
and
its
progression
have
opened
a
new
era
treatment
this
tumor.
Vemurafenib
was
first
specific
kinase
inhibitor
approved
for
therapy
advanced
melanomas
harboring
BRAF-activating
mutations,
followed
by
dabrafenib
encorafenib.
However,
despite
excellent
results
first-generation
inhibitors
terms
response
rate,
average
duration
short,
due
to
onset
genetic
epigenetic
resistance
mechanisms.
combination
with
MEK
is
an
strategy
circumvent
drug
resistance,
additional
advantage
reducing
side
effects
paradoxical
reactivation
MAPK
pathway.
recent
development
RAS
extracellular
signal-related
kinases
(ERK)
promises
add
players
ultimate
suppression
signaling
control
pathway-related
resistance.
In
review,
we
analyze
pharmacological,
preclinical,
clinical
trial
data
various
inhibitors,
keen
interest
their
applicability
management
melanoma.
International Journal of Molecular Sciences,
Journal Year:
2020,
Volume and Issue:
21(16), P. 5624 - 5624
Published: Aug. 6, 2020
Many
studies
have
revealed
a
central
role
of
p38
MAPK
in
neuronal
plasticity
and
the
regulation
long-term
changes
synaptic
efficacy,
such
as
potentiation
(LTP)
depression
(LTD).
However,
is
classically
known
responsive
element
to
stress
stimuli,
including
neuroinflammation.
Specific
pathophysiology
Alzheimer’s
disease
(AD),
several
shown
that
cascade
activated
either
response
Aβ
peptide
or
presence
tauopathies.
Here,
we
describe
its
implication
an
animal
model
neurodegeneration.
In
particular,
recent
evidence
suggests
α
isoform
potential
neurotherapeutic
target,
specific
inhibitors
been
developed
proven
be
effective
ameliorating
memory
deficits
AD
mouse
models.
Frontiers in Molecular Neuroscience,
Journal Year:
2022,
Volume and Issue:
15
Published: Aug. 25, 2022
Regulated
cell
death
(RCD)
is
an
ordered
and
tightly
orchestrated
set
of
changes/signaling
events
in
both
gene
expression
protein
activity
responsible
for
normal
development
as
well
maintenance
tissue
homeostasis.
Aberrant
activation
this
pathway
results
by
various
mechanisms
including
apoptosis,
necroptosis,
pyroptosis,
ferroptosis,
autophagy-dependent
death.
Such
pathological
changes
neurons
alone
or
combination
have
been
observed
the
pathogenesis
neurodegenerative
diseases
Alzheimer’s
disease
(AD).
Pathological
hallmarks
AD
focus
primarily
on
accumulation
two
main
markers:
amyloid
β
peptides
abnormally
phosphorylated
tau
proteins.
These
aggregates
result
formation
A-β
plaques
neuro-fibrillary
tangles
(NFTs)
induce
neuroinflammation
neurodegeneration
over
years
to
decades
leading
a
multitude
cognitive
behavioral
deficits.
Autopsy
findings
reveal
massive
neuronal
manifested
form
cortical
volume
shrinkage,
reduction
sizes
gyri
up
50%
increase
sulci.
Multiple
forms
recorded
from
different
studies
conducted
so
far.
However,
understanding
mechanism/s
patients
remains
mystery
trigger
that
aberrant
RCD
unknown
because
limited
availability
dying
neurons.
This
review
attempts
elucidate
process
death,
how
it
gets
unregulated
response
intra
extracellular
stressors,
their
interplay
role
Disease
human
experimental
models
AD.
Further
we
plan
explore
correlation
amyloid-beta
Tau
with
loss
seen
