The Role of Ferroptosis and Cuproptosis in Tuberculosis Pathogenesis: Implications for Therapeutic Strategies
Current Issues in Molecular Biology,
Год журнала:
2025,
Номер
47(2), С. 99 - 99
Опубликована: Фев. 5, 2025
Tuberculosis
(TB)
caused
by
Mycobacterium
tuberculosis
(M.tb)
remains
a
global
health
crisis,
with
over
10
million
people
affected
annually.
Despite
advancements
in
treatment,
M.tb
has
developed
mechanisms
to
evade
host
immune
responses,
complicating
efforts
eradicate
the
disease.
Two
emerging
cell
death
pathways,
ferroptosis
and
cuproptosis,
have
been
linked
TB
pathogenesis.
Ferroptosis,
an
iron-dependent
form
of
death,
is
driven
lipid
peroxidation
reactive
oxygen
species
(ROS)
accumulation.
This
process
can
limit
replication
depleting
intracellular
iron
inducing
macrophage
necrosis.
However,
excessive
may
lead
tissue
damage
aid
bacterial
dissemination.
Cuproptosis,
triggered
copper
accumulation,
disrupts
mitochondrial
metabolism,
leading
protein
aggregation
death.
exploits
both
metabolism
survive
within
macrophages,
manipulating
these
processes
resist
oxidative
stress
responses.
review
examines
roles
cuproptosis
TB,
discussing
how
manipulates
pathways
for
survival.
While
therapeutic
strategies
targeting
processes,
such
as
inducers
(Erastin,
RSL3)
inhibitors
(Ferrostatin-1)
ionophores
(Disulfiram,
Elesclomol)
chelators,
show
promise,
limited
understanding
potential
off-target
effects
significant
challenge.
Further
exploration
provide
insights
into
development
targeted
therapies
aimed
at
controlling
infection
while
minimizing
damage.
By
elucidating
complex
interactions
between
ferroptosis,
future
could
better
address
resistance
improve
clinical
outcomes.
Язык: Английский
Multi-Omics Analysis of the Immune Effect of the Engineered Exosome Drug Delivery System in Inducing Macrophage Apoptosis
Pharmaceutics,
Год журнала:
2025,
Номер
17(4), С. 494 - 494
Опубликована: Апрель 8, 2025
Background:
In
this
study,
exosomes
were
engineered
with
anti-CD47
antibody
and
loaded
rifapentine
to
improve
their
ability
target
macrophages
for
drug
delivery.
Methods:
Exosomes
from
RAW264.7
cell
supernatant
extracted
by
differential
centrifugation,
antibody-modified,
drug-loaded
ultrasonically.
After
co-culturing
macrophages,
transcriptomics
proteomics
screened
differentially
expressed
genes
proteins.
Western
Blot
identified
macrophage
polarization,
ELISA
detected
inflammatory
indicators,
an
apoptosis
kit
was
used
fluorescence
staining.
Results:
Transcriptome
sequencing
showed
that
406
in
the
changed
significantly,
pathways
like
TNF
NF-κB.
Proteomics
7478
proteins,
433
significant
differences.
indicated
M1
polarization.
Fluorescence
staining
antiMExo-RIF
group.
Conclusions:
The
study
provides
multi-omics
evidence
of
immune
mechanism
exosome
delivery
system
inducing
apoptosis,
revealing
potential
molecular
mechanisms
great
use
treating
macrophage-related
diseases.
Язык: Английский