Cell Death and Disease,
Journal Year:
2024,
Volume and Issue:
15(7)
Published: July 4, 2024
Abstract
Autoimmune
diseases
commonly
affect
various
systems,
but
their
etiology
and
pathogenesis
remain
unclear.
Currently,
increasing
research
has
highlighted
the
role
of
ferroptosis
in
immune
regulation,
with
cells
being
a
crucial
component
body’s
system.
This
review
provides
an
overview
discusses
relationship
between
ferroptosis,
programmed
cell
death
cells,
autoimmune
diseases.
Additionally,
it
summarizes
key
targets
such
as
GPX4
TFR,
responses.
Furthermore,
release
multiple
molecules,
including
damage-associated
molecular
patterns
(DAMPs),
following
by
is
examined,
these
molecules
further
influence
differentiation
function
thereby
affecting
occurrence
progression
Moreover,
secrete
factors
or
metabolites,
which
also
impact
target
organs
tissues
involved
Iron
chelators,
chloroquine
its
derivatives,
antioxidants,
calreticulin
have
been
demonstrated
to
be
effective
animal
studies
for
certain
diseases,
exerting
anti-inflammatory
immunomodulatory
effects.
Finally,
brief
summary
future
perspectives
on
are
provided,
aiming
guide
disease
treatment
strategies.
Molecular Cancer,
Journal Year:
2024,
Volume and Issue:
23(1)
Published: May 18, 2024
Abstract
Aging
and
cancer
exhibit
apparent
links
that
we
will
examine
in
this
review.
The
null
hypothesis
aging
coincide
because
both
are
driven
by
time,
irrespective
of
the
precise
causes,
can
be
confronted
with
idea
share
common
mechanistic
grounds
referred
to
as
‘hallmarks’.
Indeed,
several
hallmarks
also
contribute
carcinogenesis
tumor
progression,
but
some
molecular
cellular
characteristics
may
reduce
probability
developing
lethal
cancer,
perhaps
explaining
why
very
old
age
(>
90
years)
is
accompanied
a
reduced
incidence
neoplastic
diseases.
We
discuss
possibility
process
itself
causes
meaning
time-dependent
degradation
supracellular
functions
accompanies
produces
byproduct
or
‘age-associated
disease’.
Conversely,
its
treatment
erode
health
drive
process,
has
dramatically
been
documented
for
survivors
diagnosed
during
childhood,
adolescence,
young
adulthood.
conclude
connected
superior
including
endogenous
lifestyle
factors,
well
bidirectional
crosstalk,
together
render
not
only
risk
factor
an
important
parameter
must
considered
therapeutic
decisions.
Nature Reviews Genetics,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Aug. 12, 2024
The
DNA
methylation
field
has
matured
from
a
phase
of
discovery
and
genomic
characterization
to
one
seeking
deeper
functional
understanding
how
this
modification
contributes
development,
ageing
disease.
In
particular,
the
past
decade
seen
many
exciting
mechanistic
discoveries
that
have
substantially
expanded
our
appreciation
for
generic,
evolutionarily
ancient
can
be
incorporated
into
robust
epigenetic
codes.
Here,
we
summarize
current
distinct
landscapes
emerge
over
mammalian
lifespan
discuss
they
interact
with
other
regulatory
layers
support
diverse
functions.
We
then
review
rising
interest
in
alternative
patterns
found
during
senescence
somatic
transition
cancer.
Alongside
advancements
single-cell
long-read
sequencing
technologies,
collective
insights
made
across
these
fields
offer
new
opportunities
connect
biochemical
genetic
features
cell
physiology,
developmental
potential
phenotype.
Review,
Smith
et
al.
describe
development
within
key
disease
states,
as
well
different
methyltransferases
interface
histone
modifications
proteins
create
maintain
them.
Nutrients,
Journal Year:
2024,
Volume and Issue:
16(4), P. 496 - 496
Published: Feb. 9, 2024
Magnesium
is
an
essential
ion
in
the
human
body
that
regulates
numerous
physiological
and
pathological
processes.
deficiency
very
common
old
age.
Age-related
chronic
diseases
aging
process
itself
are
frequently
associated
with
low-grade
inflammation,
called
‘inflammaging’.
Because
magnesium
insufficiency
has
been
linked
to
excessive
generation
of
inflammatory
markers
free
radicals,
inducing
a
state,
we
formerly
hypothesized
inadequacy
may
be
considered
among
intermediaries
helping
us
explain
link
between
inflammaging
aging-associated
diseases.
We
show
this
review
evidence
relationship
all
hallmarks
(genomic
instability,
telomere
attrition,
epigenetic
alterations,
loss
proteostasis,
deregulated
nutrient
sensing,
mitochondrial
dysfunction,
cellular
senescence,
stem
cell
exhaustion,
altered
intercellular
communication,
disabled
autophagy,
dysbiosis,
inflammation),
which
positively
affect
healthspan.
It
feasible
hypothesize
maintaining
optimal
balance
during
one’s
life
course
turn
out
safe
economical
strategy
contributing
promotion
healthy
aging.
Future
well-designed
studies
necessary
further
explore
hypothesis.
MedComm – Oncology,
Journal Year:
2024,
Volume and Issue:
3(1)
Published: Jan. 4, 2024
Abstract
Epigenetic
regulation
refers
to
the
alteration
of
gene
expression
independent
changes
in
DNA
sequence.
It
involves
chemical
modifications
such
as
methylation,
histone
and
acetylation,
which
are
regulated
by
a
coordinated
interplay
various
regulators
ensure
precise
spatial
temporal
expression.
aberrations
commonly
observed
cancer
considered
hallmarks
cancer.
In
recent
years,
small
molecules
targeting
specific
epigenetic
have
been
developed
demonstrating
promising
therapeutic
potential
preclinical
clinical
trials
for
treatment.
this
review,
we
summarize
essential
regulatory
mechanisms
dysfunctions
involved
acetylation
during
tumor
development
progression.
Moreover,
discuss
current
advances
challenges
therapy
that
target
these
both
hematologic
malignancies
solid
tumors.
Finally,
combining
drugs
with
other
therapies,
including
chemotherapy,
radiotherapy,
targeted
therapy,
immunotherapy,
approach
Overall,
aim
enhance
understanding
explore
strategies
based
on
mechanisms,
ultimately
advance
improve
patient
prognosis.
MedComm,
Journal Year:
2024,
Volume and Issue:
5(2)
Published: Feb. 1, 2024
Abstract
Epigenetic
modifications
are
defined
as
heritable
changes
in
gene
activity
that
do
not
involve
the
underlying
DNA
sequence.
The
oncogenic
process
is
driven
by
accumulation
of
alterations
impact
genome's
structure
and
function.
Genetic
mutations,
which
directly
disrupt
sequence,
complemented
epigenetic
modulate
expression,
thereby
facilitating
acquisition
malignant
characteristics.
Principals
among
these
shifts
methylation
histone
mark
patterns,
promote
tumor
development
metastasis.
Notably,
reversible
nature
alterations,
opposed
to
permanence
genetic
changes,
positions
machinery
a
prime
target
discovery
novel
therapeutics.
Our
review
delves
into
complexities
regulation,
exploring
its
profound
effects
on
initiation,
metastatic
behavior,
metabolic
pathways,
microenvironment.
We
place
particular
emphasis
dysregulation
at
each
level
modulation,
including
but
limited
to,
aberrations
enzymes
responsible
for
modification,
subunit
loss
or
fusions
chromatin
remodeling
complexes,
disturbances
higher‐order
structure.
Finally,
we
also
evaluate
therapeutic
approaches
leverage
growing
understanding
dysregulation,
offering
new
avenues
cancer
treatment.
Cancer Discovery,
Journal Year:
2024,
Volume and Issue:
14(10), P. 1783 - 1809
Published: Oct. 4, 2024
Abstract
Cancer
is
a
complex
disease
in
which
several
molecular
and
cellular
pathways
converge
to
foster
the
tumoral
phenotype.
Notably,
latest
iteration
of
cancer
hallmarks,
“nonmutational
epigenetic
reprogramming”
was
newly
added.
However,
epigenetics,
much
like
genetics,
broad
scientific
area
that
deserves
further
attention
due
its
multiple
roles
initiation,
progression,
adaptive
nature.
Herein,
we
present
detailed
examination
hallmarks
affected
human
cancer,
elucidating
genes
involved,
dissecting
disrupted
landscapes
for
DNA
methylation,
histone
modifications,
chromatin
architecture
define
disease.
Significance:
characterized
by
constant
evolution,
spanning
from
initial
premalignant
stages
advanced
invasive
disseminated
stages.
It
pathology
able
adapt
survive
amidst
hostile
microenvironments
diverse
treatments
implemented
medical
professionals.
The
more
fixed
setup
genetic
structure
cannot
fully
provide
transformed
cells
with
tools
but
rapid
plastic
nature
changes
ready
task.
This
review
summarizes
ecological
success
our
bodies.
Signal Transduction and Targeted Therapy,
Journal Year:
2025,
Volume and Issue:
10(1)
Published: March 7, 2025
Redox
signaling
acts
as
a
critical
mediator
in
the
dynamic
interactions
between
organisms
and
their
external
environment,
profoundly
influencing
both
onset
progression
of
various
diseases.
Under
physiological
conditions,
oxidative
free
radicals
generated
by
mitochondrial
respiratory
chain,
endoplasmic
reticulum,
NADPH
oxidases
can
be
effectively
neutralized
NRF2-mediated
antioxidant
responses.
These
responses
elevate
synthesis
superoxide
dismutase
(SOD),
catalase,
well
key
molecules
like
nicotinamide
adenine
dinucleotide
phosphate
(NADPH)
glutathione
(GSH),
thereby
maintaining
cellular
redox
homeostasis.
Disruption
this
finely
tuned
equilibrium
is
closely
linked
to
pathogenesis
wide
range
Recent
advances
have
broadened
our
understanding
molecular
mechanisms
underpinning
dysregulation,
highlighting
pivotal
roles
genomic
instability,
epigenetic
modifications,
protein
degradation,
metabolic
reprogramming.
findings
provide
foundation
for
exploring
regulation
mechanistic
basis
improving
therapeutic
strategies.
While
antioxidant-based
therapies
shown
early
promise
conditions
where
stress
plays
primary
pathological
role,
efficacy
diseases
characterized
complex,
multifactorial
etiologies
remains
controversial.
A
deeper,
context-specific
signaling,
particularly
redox-sensitive
proteins,
designing
targeted
aimed
at
re-establishing
balance.
Emerging
small
molecule
inhibitors
that
target
specific
cysteine
residues
proteins
demonstrated
promising
preclinical
outcomes,
setting
stage
forthcoming
clinical
trials.
In
review,
we
summarize
current
intricate
relationship
disease
also
discuss
how
these
insights
leveraged
optimize
strategies
practice.