Cellular senescence in the tumor with a bone niche microenvironment: friend or foe?
Sajad Alavimanesh,
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Negar Nayerain Jazi,
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Maedeh Choubani
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et al.
Clinical and Experimental Medicine,
Journal Year:
2025,
Volume and Issue:
25(1)
Published: Jan. 23, 2025
Cellular
senescence
is
understood
to
be
a
biological
process
that
defined
as
irreversible
growth
arrest
and
was
originally
recognized
tumor-suppressive
mechanism
prevents
further
propagation
of
damaged
cells.
More
recently,
cellular
has
been
shown
have
dual
role
in
prevention
tumor
promotion.
Senescent
cells
carry
senescence-associated
secretory
phenotype
(SASP),
which
altered
by
factors
including
pro-inflammatory
cytokines,
chemokines,
other
proteases,
leading
the
alteration
tissue
microenvironment.
Though
would
eventually
halt
cancerous
potential
cells,
SASP
contributes
environment
promoting
inflammation,
matrix
remodeling,
cell
invasion.
The
paradox
prevention/promotion
particularly
relevant
bone
niche
microenvironment,
where
longer-lasting,
chronic
inflammation
promotes
formation.
Insights
into
mechanistic
understanding
provide
basis
for
targeted
therapies,
such
senolytics,
aim
eliminate
senescent
or
inhibitors,
tumor-promoting
effects
senescence.
These
therapeutic
interventions
offer
significant
clinical
implications
treating
cancer
healthy
aging.
Language: Английский
Neuroimmune crosstalk in chronic neuroinflammation: microglial interactions and immune modulation
Ludmila Müller,
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Svetlana Di Benedetto
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Frontiers in Cellular Neuroscience,
Journal Year:
2025,
Volume and Issue:
19
Published: April 7, 2025
Neuroinflammation
is
a
fundamental
feature
of
many
chronic
neurodegenerative
diseases,
where
it
contributes
to
disease
onset,
progression,
and
severity.
This
persistent
inflammatory
state
arises
from
the
activation
innate
adaptive
immune
responses
within
central
nervous
system
(CNS),
orchestrated
by
complex
interplay
resident
cells,
infiltrating
peripheral
an
array
molecular
mediators
such
as
cytokines,
chemokines,
extracellular
vesicles.
Among
CNS-resident
microglia
play
role,
exhibiting
dynamic
spectrum
phenotypes
ranging
neuroprotective
neurotoxic.
In
sustained
microglial
often
leads
amplification
cascades,
reinforcing
pathogenic
cycle
immune-mediated
damage.
Intercellular
communication
inflamed
CNS
persistence
progression
neuroinflammation.
Microglia
engage
in
extensive
crosstalk
with
astrocytes,
neurons,
oligodendrocytes,
shaping
both
local
systemic
responses.
These
interactions
influence
key
processes
synaptic
pruning,
phagocytosis,
blood-brain
barrier
integrity,
cytokine-mediated
signaling.
Understanding
mechanisms
cell-cell
signaling
this
context
critical
for
identifying
therapeutic
strategies
modulate
response
restore
homeostasis.
review
explores
players
neuroinflammation,
focus
on
role
microglia,
pathways
underlying
intercellular
communication,
potential
approaches
mitigate
neuroinflammatory
damage
diseases.
Language: Английский
Immunosenescence in digestive system cancers: mechanisms, research advances, and therapeutic strategies
Junyan Zhang,
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Xiaojiao Guan,
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Xinwen Zhong
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et al.
Seminars in Cancer Biology,
Journal Year:
2024,
Volume and Issue:
106-107, P. 234 - 250
Published: Nov. 1, 2024
Language: Английский
Antioxidant Features of Humic Products by ABTS Assay
Methods in molecular biology,
Journal Year:
2024,
Volume and Issue:
unknown, P. 223 - 227
Published: Sept. 30, 2024
Language: Английский
RNA sequencing comparing centenarian and middle‐aged women lymphoblastoid cell lines identifies age‐related dysregulated expression of genes encoding selenoproteins, heat shock proteins, CD99, and BID
Irena Voinsky,
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Ofir Goldenberg‐Bogner,
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Ifat Israel‐Elgali
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et al.
Drug Development Research,
Journal Year:
2024,
Volume and Issue:
85(7)
Published: Oct. 24, 2024
Abstract
Women
typically
live
longer
than
men,
and
constitute
the
majority
of
centenarians.
We
applied
RNA‐sequencing
(RNA‐seq)
blood‐derived
lymphoblastoid
cell
lines
(LCLs)
from
women
aged
60‐80
years
centenarians
(100‐105
years),
validated
RNA‐seq
findings
by
real‐time
PCR,
additionally
measured
differentially
expressed
genes
in
LCLs
young
20‐35
years.
Top
with
differential
expression
between
age
groups
included
three
selenoproteins
(
GPX1,
SELENOW,
SELENOH
)
heat
shock
proteins
HSPA6,
HSPA1A,
HSPA1B
),
highest
women,
indicating
that
are
better
protected
oxidative
stress.
The
two
additional
genes,
BID
encoding
BH3‐interacting
domain
death
agonist
CD99
antigen,
showed
unique
dependence,
similar
levels
centenarian
while
exhibiting
higher
lower
levels,
respectively,
compared
other
groups.
This
age‐related
suggests
elevated
inflammation
susceptibility
middle‐aged
either
or
women.
Our
findings,
once
human
peripheral
blood
mononuclear
cells
further
types,
may
lead
to
novel
healthy
aging
diagnostics
therapeutics.
Language: Английский