Mechanisms of radiation‐induced tissue damage and response
Zhou Lin,
No information about this author
Jiaojiao Zhu,
No information about this author
Yuhao Liu
No information about this author
et al.
MedComm,
Journal Year:
2024,
Volume and Issue:
5(10)
Published: Sept. 20, 2024
Radiation-induced
tissue
injury
(RITI)
is
the
most
common
complication
in
clinical
tumor
radiotherapy.
Due
to
heterogeneity
response
of
different
tissues
radiation
(IR),
radiotherapy
will
cause
types
and
degrees
RITI,
which
greatly
limits
application
Efforts
are
continuously
ongoing
elucidate
molecular
mechanism
RITI
develop
corresponding
prevention
treatment
drugs
for
RITI.
Single-cell
sequencing
(Sc-seq)
has
emerged
as
a
powerful
tool
uncovering
mechanisms
identifying
potential
targets
by
enhancing
our
understanding
complex
intercellular
relationships,
facilitating
identification
novel
cell
phenotypes,
allowing
assessment
spatiotemporal
developmental
trajectories.
Based
on
comprehensive
review
we
analyzed
regulatory
networks
combination
with
Sc-seq
summarized
targeted
intervention
pathways
therapeutic
Deciphering
diverse
underlying
can
shed
light
its
pathogenesis
unveil
new
avenues
potentially
facilitate
repair
or
regeneration
currently
irreversible
Furthermore,
discuss
how
personalized
strategies
based
offer
promise
mitigating
Language: Английский
Comparative Analysis of Phytochemical Constituents of Ginkgo Biloba Flowers and Leaves, and Evaluation of Their Biological Activities
Published: Jan. 1, 2025
Ginkgo
biloba
L,
as
a
Mesozoic
relict
tree
species
specialized
in
China,
has
attracted
much
attention
for
its
unique
chemical
composition
and
pharmacological
properties,
most
of
the
research
focused
on
leaves
(GBL).
Our
preliminary
found
that
flowers
(GBF)
were
superior
to
GBL
terms
anti-radiation
activity,
but
underlying
cause
this
discrepancy
activity
remains
elusive.
Therefore,
present
study
aimed
systematically
compare
nutritional
compositions
GBF
investigate
intrinsic
mechanism
their
activities.In
study,
constituents
identified
by
UPLC-Q-orbitrap
HRMS,
contents
amino
acids,
fatty
inorganic
elements,
purines,
ceramides
both
determined.
Meanwhile,
activities
exerted
through
regulation
ferroptosis
compared,
focusing
effect
inhibiting
ferroptosis.The
results
showed
was
indeed
anti-ferroptosis
exhibited
more
significant
inhibitory
regulating
ferroptosis.
Through
in-depth
analyses
both,
reveals
possible
material
basis
stronger
provides
theoretical
support
application
nutraceuticals
pharmaceuticals,
especially
development
functional
drugs
with
higher
health
benefits.
Language: Английский
BUB1 Inhibition Induces Ferroptosis in Triple-Negative Breast Cancer Cell Lines
Sushmitha Sriramulu,
No information about this author
Shivani Thoidingjam,
No information about this author
Stephen L. Brown
No information about this author
et al.
DNA,
Journal Year:
2025,
Volume and Issue:
5(1), P. 16 - 16
Published: March 12, 2025
Background:
Triple-negative
breast
cancer
(TNBC)
is
a
highly
aggressive
subtype
with
limited
effective
treatments
available,
including
targeted
therapies,
often
leading
to
poor
prognosis.
Mitotic
checkpoint
kinase
BUB1
frequently
overexpressed
in
TNBC
and
correlates
survival
outcomes
suggesting
its
potential
as
therapeutic
target.
This
study
explores
the
cytotoxicity
of
cells
inhibition,
alone
or
combination
radiation
demonstrates
that
ferroptosis,
an
iron-dependent
form
programmed
cell
death,
has
role.
Methods:
lines
(SUM159,
MDA-MB-231,
BT-549)
were
treated
inhibitor
BAY1816032
(BUB1i)
ferroptosis
activator
RSL3
without
4
Gy
irradiation.
Cell
viability
assays
conducted
assess
treatment
effects,
qPCR
analyses
measured
expression
key
markers
ACSL4,
GPX4,
PTGS2,
SLC7A11,
NCOA4,
IREB2,
NFS1,
TFRC
expression,
TBARS
assay
lipid
peroxidation
levels.
Ferroptosis
specificity
was
confirmed
through
co-treatment
Ferrostatin-1
(F-1).
Results:
In
all
studied,
inhibition
significantly
induced
marked
by
increased
ACSL4
decreased
GPX4
The
BUB1i
further
amplified
these
ferroptotic
markers,
at
least
additive
effect,
which
not
present
radiation.
Co-treatment
reversed
BUB1i-mediated
death
may
involve
signaling
lines.
Conclusions:
independently
induce
lines,
enhanced
when
combined
activator.
Further
research
warranted
delineate
molecular
mechanism
BUB1-mediated
TNBC.
Language: Английский