Advanced Materials,
Journal Year:
2024,
Volume and Issue:
36(27)
Published: April 19, 2024
Abstract
Advancing
biofabrication
toward
manufacturing
living
constructs
with
well‐defined
architectures
and
increasingly
biologically
relevant
cell
densities
is
highly
desired
to
mimic
the
biofunctionality
of
native
human
tissues.
The
formulation
tissue‐like,
cell‐dense
inks
for
remains,
however,
challenging
at
various
levels
bioprinting
process.
Promising
advances
have
been
made
this
goal,
achieving
relatively
high
that
surpass
those
found
in
conventional
platforms,
pushing
current
boundaries
closer
tissue‐like
densities.
On
focus,
herein
overarching
challenges
bioprocessing
cell‐rich
into
clinically
grade
engineered
tissues
are
discussed,
as
well
most
recent
ink
formulations
their
processing
technologies
highlighted.
Additionally,
an
overview
foreseen
developments
field
provided
critically
discussed.
Journal of Translational Medicine,
Journal Year:
2025,
Volume and Issue:
23(1)
Published: Jan. 22, 2025
Cuproptosis
differs
from
other
forms
of
cell
death,
such
as
apoptosis,
necroptosis,
and
ferroptosis,
in
its
unique
molecular
mechanisms
signaling
pathways.
In
this
review,
we
delve
into
the
cellular
metabolic
pathways
copper,
highlighting
role
copper
biomolecule
synthesis,
mitochondrial
respiration,
antioxidant
defense.
Furthermore,
elucidate
relationship
between
cuproptosis-related
genes
(CRGs)
cancer
prognosis,
analyzing
their
expression
patterns
across
various
tumor
types
impact
on
patient
outcomes.
Our
review
also
uncovers
potential
therapeutic
applications
chelators,
ionophores,
copper-based
nanomaterials
oncology.
addition,
discuss
emerging
cuproptosis
remodeling
microenvironment,
enhancing
immune
infiltration,
converting
"cold
tumors"
"hot
that
respond
better
to
immunotherapy.
short,
underscores
pivotal
importance
biology
highlights
translational
a
novel
target.
Antioxidants,
Journal Year:
2025,
Volume and Issue:
14(1), P. 108 - 108
Published: Jan. 18, 2025
The
study
of
mitochondrial
dysfunction
has
become
increasingly
pivotal
in
elucidating
the
pathophysiology
various
cerebral
pathologies,
particularly
neurodegenerative
disorders.
Mitochondria
are
essential
for
cellular
energy
metabolism,
regulation
reactive
oxygen
species
(ROS),
calcium
homeostasis,
and
execution
apoptotic
processes.
Disruptions
function,
driven
by
factors
such
as
oxidative
stress,
excitotoxicity,
altered
ion
balance,
lead
to
neuronal
death
contribute
cognitive
impairments
several
brain
diseases.
Mitochondrial
can
arise
from
genetic
mutations,
ischemic
events,
hypoxia,
other
environmental
factors.
This
article
highlights
critical
role
progression
diseases
discusses
need
targeted
therapeutic
strategies
attenuate
damage,
restore
enhance
neuroprotection.
Redox Biology,
Journal Year:
2023,
Volume and Issue:
69, P. 103008 - 103008
Published: Dec. 20, 2023
Focal
iron
overload
is
frequently
observed
in
patients
with
rheumatoid
arthritis
(RA),
yet
its
functional
significance
remains
elusive.
Herein,
we
report
that
deposition
lesion
aggravates
by
inducing
macrophage
ferroptosis.
We
show
excessive
synovial
fluid
positively
correlates
RA
disease
severity
as
does
lipid
hyperoxidation
of
focal
monocyte/macrophages.
Further
study
reveals
high
susceptibility
to
induced
ferroptosis
the
anti-inflammatory
macrophages
M2,
while
pro-inflammatory
M1
are
less
affected.
Distinct
glutathione
peroxidase
4
(GPX4)
degradation
depending
on
p62/SQSTM1
two
cell
types
make
great
contribution
mechanically.
Of
note,
inhibitor
liproxstatin-1
(LPX-1)
can
alleviate
progression
K/BxN
serum-transfer
(STIA)
mice
accompanied
increasing
M2
proportion.
thus
propose
heterogeneous
subtypes
well
consequent
inflammation
and
immune
disorders
potential
biomarkers
therapeutic
targets
RA.
Frontiers in Cell and Developmental Biology,
Journal Year:
2024,
Volume and Issue:
12
Published: Jan. 31, 2024
The
current
situation
of
hepatocellular
carcinoma
(HCC)
management
is
challenging
due
to
its
high
incidence,
mortality,
recurrence
and
metastasis.
Recent
advances
in
gene
genetic
expression
regulation
have
unveiled
the
significant
role
non-coding
RNA
(ncRNA)
various
cancers.
This
led
formulation
competing
endogenous
(ceRNA)
hypothesis,
which
posits
that
both
coding
ncRNA,
containing
miRNA
response
elements
(MRE),
can
share
same
sequence.
results
a
competitive
network
between
ncRNAs,
such
as
lncRNA
mRNA,
allowing
them
regulate
each
other.
Extensive
research
has
highlighted
crucial
ceRNA
HCC
development,
impacting
cellular
processes
including
proliferation,
metastasis,
cell
death,
angiogenesis,
tumor
microenvironment,
organismal
immunity,
chemotherapy
resistance.
Additionally,
network,
mediated
by
or
circRNA,
offers
potential
early
diagnosis
prevention
HCC.
Consequently,
ceRNAs
are
emerging
therapeutic
targets
for
complexity
these
networks
aligns
with
multi-target
approach
traditional
Chinese
medicine
(TCM),
presenting
novel
perspective
TCM
combating
Research
beginning
show
compounds
prescriptions
affect
progression
through
inhibiting
proliferation
inducing
apoptosis.
Currently,
lncRNAs
TUG1,
NEAT1,
CCAT1,
along
their
associated
networks,
among
most
promising
ncRNAs
research.
However,
this
field
still
infancy,
necessitating
advanced
technology
extensive
basic
fully
understand
mechanisms
treatment.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
14
Published: Jan. 12, 2024
Programmed
cell
death
(PCD)
is
an
evolutionarily
conserved
mechanism
of
suicide
that
controlled
by
various
signaling
pathways.
PCD
plays
important
role
in
a
multitude
biological
processes,
such
as
turnover,
development,
tissue
homeostasis
and
immunity.
Some
forms
PCD,
including
apoptosis,
autophagy-dependent
death,
pyroptosis,
ferroptosis
necroptosis,
contribute
to
carcinogenesis
cancer
thus
have
attracted
increasing
attention
the
field
oncology.
Recently,
research-based
evidence
has
demonstrated
acts
critical
modulator
tumor
can
affect
function
innate
adaptive
immune
cells,
which
leads
distinct
immunological
consequences,
priming
tumor-specific
T
immunosuppression
evasion.
Targeting
alone
or
combination
with
conventional
immunotherapy
may
provide
new
options
enhance
clinical
efficacy
anticancer
therapeutics.
In
this
review,
we
introduce
characteristics
mechanisms
ubiquitous
pathways
(e.g.,
pyroptosis
ferroptosis)
explore
complex
interaction
between
these
immunity
based
on
currently
available
evidence.
We
also
discuss
therapeutic
potential
PCD-based
approaches
outlining
trials
targeting
treatment.
Elucidating
immune-related
effects
pathogenesis
will
likely
improved
understanding
oncoimmunology
allow
be
exploited
for
Experimental & Molecular Medicine,
Journal Year:
2024,
Volume and Issue:
56(4), P. 870 - 876
Published: April 2, 2024
Abstract
Cell
death
pathways
play
critical
roles
in
organism
development
and
homeostasis
as
well
the
pathogenesis
of
various
diseases.
While
studies
over
last
decade
have
elucidated
numerous
different
forms
cell
that
can
eliminate
cells
contexts,
how
certain
mechanisms
impact
physiology
is
still
not
understood.
Moreover,
recent
shown
multiple
occur
a
population,
with
eliminating
individual
cells.
Here,
we
aim
to
describe
known
molecular
entosis,
non-apoptotic
engulfment
process,
discuss
signaling
control
its
induction
possible
crosstalk
other
mechanisms.
Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
14
Published: Jan. 5, 2024
Cancer
cells
evolve
to
be
refractory
the
intrinsic
programmed
cell
death
mechanisms,
which
ensure
cellular
tissue
homeostasis
in
physiological
conditions.
Chemotherapy
using
cytotoxic
drugs
seeks
eliminate
cancer
but
spare
non-cancerous
host
by
exploring
a
likely
subtle
difference
between
malignant
and
benign
cells.
Presumably,
chemotherapy
agents
achieve
efficacy
triggering
machineries
Currently,
many
major
solid
tumors
are
treated
with
composed
of
combination
platinum
taxanes.
Platinum
agents,
largely
cis-platin,
carboplatin,
oxaliplatin,
DNA
damaging
that
covalently
form
addicts,
repair
response
pathways.
Taxanes,
including
paclitaxel,
docetaxel,
cabazitaxel,
microtubule
stabilizing
often
very
effective
purging
clinical
settings.
Generally,
it
is
thought
stabilization
microtubules
taxanes
leads
mitotic
arrest,
catastrophe,
apoptotic
death.
However,
precise
mechanism(s)
how
arrest
catastrophe
activate
caspase
pathway
has
not
been
established.
Here,
we
briefly
review
literature
on
involvement
potential
mechanisms
therapy.
These
include
classical
caspase-mediated
death,
necroptosis
mediated
MLKL,
pore
forming
immune
cells,
etc.
In
particular,
discuss
newly
recognized
mechanism
taxane-treatment
involves
micronucleation
irreversible
rupture
nuclear
membrane.
Since
commonly
retarded
responding
signaling,
stabilized
bundle-induced
membrane
rupture,
rather
than
apoptosis,
may
key
accounting
for
success
as
anti-cancer
agents.
