Scientific Reports,
Journal Year:
2024,
Volume and Issue:
14(1)
Published: July 23, 2024
Abstract
The
liver
carries
out
many
essential
tasks,
such
as
synthesising
cholesterol,
controlling
the
body’s
storage
of
glycogen,
and
detoxifying
metabolites,
in
addition
to
performing,
regulating
homeostasis.
Hepatic
fibrosis
is
a
pathological
state
characterized
by
over
accumulation
extracellular
matrix
(ECM)
including
collagen
fibers.
Sildenafil
(a
selective
inhibitor
type
5
phosphodiesterase)
has
anti-inflammatory,
antioxidant
anti-apoptotic
properties.
It
commonly
used
treat
erectile
dysfunction
male.
purpose
current
investigation
was
evaluate
sildenafil’s
hepatoprotective
potential
against
rats
that
caused
carbon
tetrachloride
(CCl
4
).
Liver
enzymes
oxidative
markers
well
profibrotic
genes
were
determined.
findings
showed
sildenafil
alleviates
hepatic
dysfunctions
CCl
restoring
normal
levels
ALT,
AST,
GGT
status
demonstrated
increased
glutathione
(GSH),
catalase.
In
addition,
significantly
down-regulated
mRNA
expressions
[collagen-1α,
IL-1β,
osteopontin
(OPN),
transforming
growth
factor-β
(TGF-β)].
Additionally,
lessens
periportal
between
lobules,
congestion
dilatation
central
vein,
inflammatory
cell
infiltrations.
As
result,
it
hypothesized
may
be
helpful
management
hepatotoxicity
brought
on
through
suppressing
OPN.
Signal Transduction and Targeted Therapy,
Journal Year:
2023,
Volume and Issue:
8(1)
Published: Dec. 10, 2023
Abstract
Ferroptosis,
a
unique
modality
of
cell
death
with
mechanistic
and
morphological
differences
from
other
modes,
plays
pivotal
role
in
regulating
tumorigenesis
offers
new
opportunity
for
modulating
anticancer
drug
resistance.
Aberrant
epigenetic
modifications
posttranslational
(PTMs)
promote
resistance,
cancer
progression,
metastasis.
Accumulating
studies
indicate
that
can
transcriptionally
translationally
determine
vulnerability
to
ferroptosis
functions
as
driver
nervous
system
diseases
(NSDs),
cardiovascular
(CVDs),
liver
diseases,
lung
kidney
diseases.
In
this
review,
we
first
summarize
the
core
molecular
mechanisms
ferroptosis.
Then,
roles
processes,
including
histone
PTMs,
DNA
methylation,
noncoding
RNA
regulation
such
phosphorylation,
ubiquitination,
SUMOylation,
acetylation,
ADP-ribosylation,
are
concisely
discussed.
The
PTMs
genesis
cancers,
NSD,
CVDs,
well
application
PTM
modulators
therapy
these
then
discussed
detail.
Elucidating
mediated
by
will
facilitate
development
promising
combination
therapeutic
regimens
containing
or
PTM-targeting
agents
inducers
be
used
overcome
chemotherapeutic
resistance
could
prevent
addition,
highlight
potential
approaches
chemoresistance
halt
Phytomedicine,
Journal Year:
2023,
Volume and Issue:
114, P. 154762 - 154762
Published: March 14, 2023
Alzheimer's
disease
(AD)
is
a
neurogenerative
and
remains
no
effective
method
for
stopping
its
progress.
Ferroptosis
adaptive
immunity
have
been
proven
to
contribute
AD
pathogenesis.
Salidroside
exhibits
neuroprotective
immunomodulatory
effects.
However,
the
underlying
mechanisms
linking
salidroside,
ferroptosis,
in
remain
uncertain.The
objective
of
this
study
explore
effects
potential
molecular
salidroside
against
neuronal
ferroptosis
CD8+
T
cell
infiltration
senescence-accelerated
mouse
prone
8
(SAMP8)
mice.SAMP8
mice
were
employed
as
an
model
treated
with
12
weeks.
Behavioral
tests,
immunohistochemistry,
HE
Nissl
staining,
immunofluorescence,
transmission
electron
microscopy,
quantitative
proteomics,
bioinformatic
analysis,
flow
cytometry,
iron
western
blotting,
docking
performed.Treatment
dose-dependently
attenuated
cognitive
impairment,
reduced
accumulation
Aβ
plaques
restored
damage.
also
suppressed
CD8+T
cells,
oxidative
stress,
inflammatory
cytokines,
improved
mitochondrial
metabolism,
lipid
redox
SAMP8
brain.
The
administration
decreased
deposition,
TFR1,
ACSL4
protein
expression,
upregulated
SLC7A11,
GPX4
promoted
Nrf2/GPX4
axis
activation.In
conclusion,
cells
are
involved
process
impairment
mice.
alleviates
inhibits
ferroptosis.
may
involve
activation
reduction
infiltration.
This
provides
some
evidence
roles
Frontiers in Bioscience-Landmark,
Journal Year:
2024,
Volume and Issue:
29(6), P. 221 - 221
Published: June 20, 2024
The
endoplasmic
reticulum
(ER)
played
an
important
role
in
the
folding,
assembly
and
post-translational
modification
of
proteins.
ER
homeostasis
could
be
disrupted
by
accumulation
misfolded
proteins,
elevated
reactive
oxygen
species
(ROS)
levels,
abnormal
Ca2+
signaling,
which
was
referred
to
stress
(ERS).
Ferroptosis
a
unique
programmed
cell
death
model
mediated
iron-dependent
phospholipid
peroxidation
multiple
signaling
pathways.
changes
mitochondrial
structure,
damage
glutathione
peroxidase
4
(GPX4)
excess
iron
were
main
characteristics
ferroptosis.
ROS
produced
ferroptosis
can
interfere
with
activity
protein-folding
enzymes,
leading
large
amounts
unfolded
thus
causing
ERS.
On
contrary,
increase
ERS
level
promote
ion
lipid
peroxide,
up-regulation
related
genes.
At
present,
studies
on
relationship
between
one-sided
lack
in-depth
interaction
mechanism.
This
review
aimed
explore
molecular
mechanism
cross-talk
ERS,
provide
new
strategies
targets
for
treatment
liver
diseases.
