Molecules and Cells,
Год журнала:
2022,
Номер
45(9), С. 610 - 619
Опубликована: Авг. 19, 2022
Cellular
senescence
plays
a
paradoxical
role
in
tumorigenesis
through
the
expression
of
diverse
senescence-associated
(SA)
secretory
phenotypes
(SASPs).The
heterogeneity
SA
gene
cancer
cells
not
only
promotes
stemness
but
also
protects
these
from
chemotherapy.Despite
potential
correlation
between
and
biomarkers,
many
transcriptional
changes
across
distinct
cell
populations
remain
largely
unknown.During
past
decade,
single-cell
RNA
sequencing
(scRNA-seq)
technologies
have
emerged
as
powerful
experimental
analytical
tools
to
dissect
such
senescence-derived
changes.Here,
we
review
recent
efforts
that
successfully
characterized
scRNA-seq
data
obtained
elucidated
senescent
tumor
malignancy.We
further
highlight
functional
implications
genes
expressed
specifically
stromal
microenvironment.Translational
research
leveraging
profiling
will
facilitate
identification
novel
patterns
underlying
susceptibility,
providing
new
therapeutic
opportunities
era
precision
medicine.
Molecular & Cellular Proteomics,
Год журнала:
2024,
Номер
23(9), С. 100830 - 100830
Опубликована: Авг. 14, 2024
The
study
of
the
cellular
secretome
using
proteomic
techniques
continues
to
capture
attention
research
community
across
a
broad
range
topics
in
biomedical
research.
Due
their
untargeted
nature,
independence
from
model
system
used,
historically
superior
depth
analysis,
as
well
comparative
affordability,
mass
spectrometry-based
approaches
traditionally
dominate
such
analyses.
More
recently,
however,
affinity-based
assays
have
massively
gained
analytical
depth,
which
together
with
high
sensitivity,
dynamic
coverage
throughput
capabilities
render
them
exquisitely
suited
analysis.
In
this
review,
we
revisit
challenges
implied
by
secretomics
and
provide
an
overview
platforms
currently
available
for
analyses,
tumor
example
basic
translational
Expert Review of Anticancer Therapy,
Год журнала:
2022,
Номер
22(9), С. 915 - 926
Опубликована: Июль 11, 2022
Introduction
Immunosenescence
is
a
progressive
remodeling
of
immune
functions
associated
with
decreased
ability
the
system
to
set
up
an
efficient
response,
both
innate
and
adaptive,
increase
highly
differentiated
T
cells
at
expense
naive
cells.
The
incidence
prevalence
most
cancers
age,
which
can
partly
be
explained
by
tumor
escape
mechanisms
immunosurveillance.
Aging
also
inflammaging,
low-grade
proinflammatory
state
characterized
in
inflammatory
mediators.
Anti-cancer
immunotherapy
has
profoundly
changed
landscape
oncology
therapy
last
10
years.
Modern
T-cell
targeted
therapies
such
as
bispecific
cell
engagers,
CAR-T
cells,
or
checkpoint
blockers
may
theoretically
affected
immunosenescence
inflammaging.Areas
covered
A
bibliographic
review
through
PubMed
Embase
was
carried
out
using
following
search
terms:
'immunosenescence,'
'immunotherapy,'
'inflammaging,'
'bispecific
antibodies,'
'CAR-T
cells,'
'immune
blockers,'
'older
patients.'Expert
opinion
This
explores
potential
impact
inflammaging
on
anti-cancer
therapeutic
strategies
that
could
counter
senescence.
more
dedicated
research
biomarkers
future
clinical
trials
warranted
for
development
new,
effective
safer
therapies.
Journal of Blood Medicine,
Год журнала:
2024,
Номер
Volume 15, С. 313 - 323
Опубликована: Июль 1, 2024
Abstract:
Sickle
Cell
Anemia
(SCA)
is
a
hereditary
blood
disorder
characterized
by
the
presence
of
abnormal
hemoglobin,
leading
to
formation
sickle-shaped
red
cells.
While
extensive
research
has
unraveled
many
aspects
genetic
and
molecular
basis
SCA,
role
telomere
dynamics
in
disease
progression
remains
relatively
unexplored
frontier.
This
review
seeks
provide
comprehensive
examination
biology
within
context
aiming
elucidate
its
potential
impact
on
aging
disease.
The
oxidative
stress
SCA
explored,
with
particular
focus
how
increased
reactive
oxygen
species
(ROS)
may
contribute
accelerated
shortening
genomic
instability.
Furthermore,
relationship
between
dysfunction
cellular
senescence
investigated,
shedding
light
premature
cells
this
population.
concludes
summarizing
key
findings
proposing
therapeutic
strategies
targeting
mitigate
SCA.
It
also
identifies
gaps
current
understanding
suggests
avenues
for
future
research,
emphasizing
importance
further
investigating
advance
our
Anemia.
exploration
offers
insights
into
mechanisms
progression,
paving
way
targeted
interventions
improved
management.
Keywords:
sickle
cell
anemia,
telomere,
aging,
hemoglobinopathy,
shortening,
Cells,
Год журнала:
2022,
Номер
11(3), С. 541 - 541
Опубликована: Фев. 4, 2022
A
plethora
of
factors
have
been
attributed
to
underly
aging,
including
oxidative
stress,
telomere
shortening
and
cellular
senescence.
Several
studies
shown
a
significant
role
the
cyclin-dependent
kinase
inhibitor
p16ink4a
in
senescence
aging.
However,
its
expression
development
has
less
well
documented.
Therefore,
further
clarify
potential
p16
we
conducted
developmental
study
p16,
as
p19ARF
p21,
investigated
their
on
RNA
level
brain,
heart,
liver,
kidney
mice
at
embryonic,
postnatal,
adult,
old
ages.
P16
was
assessed
protein
by
immunohistochemistry.
Expression
highly
dynamic
all
organs
embryonic
postnatal
stages
increased
dramatically
mice.
p19
p21
variable
moderate
extent
age.
In
addition,
observed
predominant
mRNA
liver
endothelial
cells
versus
non-endothelial
mice,
which
suggests
functional
specifically
endothelium
subjects.
Thus,
spatiotemporal
might
implicate
physiological
processes
addition
well-known
function
build-up
Journal of Neuroinflammation,
Год журнала:
2024,
Номер
21(1)
Опубликована: Апрель 5, 2024
Abstract
Background
It
is
well
established
that
traumatic
brain
injury
(TBI)
causes
acute
and
chronic
alterations
in
systemic
immune
function
changes
contribute
to
posttraumatic
neuroinflammation
neurodegeneration.
However,
how
TBI
affects
bone
marrow
(BM)
hematopoietic
stem/progenitor
cells
chronically
what
extent
such
may
negatively
impact
innate
immunity
neurological
has
not
been
examined.
Methods
To
further
understand
the
role
of
BM
cell
derivatives
on
outcome,
we
generated
chimeric
mice
by
transplanting
from
injured
or
sham
(i.e.,
90
days
post-surgery)
congenic
donor
into
otherwise
healthy,
age-matched,
irradiated
CD45.2
C57BL/6
(WT)
hosts.
Immune
were
evaluated
flow
cytometry,
multiplex
ELISA,
NanoString
technology.
Moderate-to-severe
was
induced
controlled
cortical
measured
using
a
battery
behavioral
tests.
Results
transcriptome
lineage
−
c-Kit
+
Sca1
(LSK+)
mice,
including
modified
epigenetic
senescence
pathways.
After
8
weeks
reconstitution,
peripheral
myeloid
TBI→WT
showed
significantly
higher
oxidative
stress
levels
reduced
phagocytic
activity.
At
eight
months
after
leukopenic,
with
continued
phagocytosis
responses,
as
persistent
deficits.
Gene
expression
analysis
revealed
BM-driven
neuropathology
respectively.
Chimeric
subjected
at
post-reconstitution
longer
reconstitution
periods
time
post-injury)
associated
increased
microgliosis
leukocyte
infiltration.
Pre-treatment
senolytic
agent,
ABT-263,
improved
performance
aged
baseline,
although
it
did
attenuate
acutely
brain.
Conclusions
activation
progressive
dysfunction
pool,
which
drives
long-term
deficits
hematopoiesis,
immunity,
function,
altered
sensitivity
subsequent
injury.
Aging and Disease,
Год журнала:
2024,
Номер
unknown, С. 0 - 0
Опубликована: Янв. 1, 2024
This
comprehensive
review
navigates
the
complex
relationship
between
cellular
aging,
senescence,
and
cancer,
unraveling
determinants
of
fate.
Beginning
with
an
overview
aging's
significance
in
explores
processes,
changes,
molecular
pathways
influencing
senescence.
The
senescence
as
a
dual
mechanism
acting
suppressor
contributor,
focusing
on
its
impact
therapy
response.
highlights
opportunities
for
cancer
therapies
that
target
further
examines
senescence-associated
secretory
phenotype
strategies
to
modulate
aging
influence
tumor
behavior.
Additionally,
mechanisms
escape
cells,
emphasizing
their
prognosis
resistance
therapy.
article
addresses
current
advances,
unexplored
aspects,
future
perspectives
understanding
cancer.
