Biology,
Год журнала:
2025,
Номер
14(2), С. 131 - 131
Опубликована: Янв. 27, 2025
Extrapulmonary
tuberculosis
(EPTB)
accounts
for
approximately
17%
of
all
Mycobacterium
(M.tb)
infections
globally.
Immunocompromised
individuals,
such
as
those
with
HIV
infection
or
type
2
diabetes
mellitus
(T2DM),
are
at
an
increased
risk
EPTB.
Previous
studies
have
demonstrated
that
patients
and
T2DM
exhibit
diminished
synthesis
glutathione
(GSH)
synthesizing
enzymes.
In
a
murine
model,
we
showed
the
diethyl
maleate
(DEM)-induced
depletion
GSH
in
lungs
led
to
M.tb
burden
impaired
pulmonary
granulomatous
response
infection.
However,
effects
during
active
EPTB
liver
spleen
yet
be
elucidated.
this
study,
evaluated
hepatic
malondialdehyde
(MDA)
levels,
well
cytokine
profiles,
untreated
DEM-treated
M.tb-infected
wild-type
(WT)
C57BL/6
mice.
Additionally,
assessed
splenic
burdens
tissue
pathologies.
DEM
treatment
resulted
significant
decrease
levels
reduced
form
increase
MDA,
oxidized
GSH,
interleukin
(IL)-6
levels.
Furthermore,
DEM-induced
was
associated
decreased
production
IL-12
IL-17
elevated
interferon-gamma
(IFN-γ),
tumor
necrosis
factor
(TNF)-α,
transforming
growth
(TGF)-β.
A
detected
Large,
disorganized
lymphocyte
infiltrates
were
tissues
Overall,
diminishment
exacerbated
both
spleen.
These
findings
provide
critical
insights
into
immunomodulatory
role
TB
pathogenesis
suggest
potential
therapeutic
avenues
extrapulmonary
infections.
Molecular Biomedicine,
Год журнала:
2023,
Номер
4(1)
Опубликована: Окт. 16, 2023
Abstract
Ferroptosis,
a
regulated
form
of
cellular
death
characterized
by
the
iron-mediated
accumulation
lipid
peroxides,
provides
novel
avenue
for
delving
into
intersection
metabolism,
oxidative
stress,
and
disease
pathology.
We
have
witnessed
mounting
fascination
with
ferroptosis,
attributed
to
its
pivotal
roles
across
diverse
physiological
pathological
conditions
including
developmental
processes,
metabolic
dynamics,
oncogenic
pathways,
neurodegenerative
cascades,
traumatic
tissue
injuries.
By
unraveling
intricate
underpinnings
molecular
machinery,
contributors,
signaling
conduits,
regulatory
networks
governing
researchers
aim
bridge
gap
between
intricacies
this
unique
mode
multifaceted
implications
health
disease.
In
light
rapidly
advancing
landscape
ferroptosis
research,
we
present
comprehensive
review
aiming
at
extensive
in
origins
progress
human
diseases.
This
concludes
careful
analysis
potential
treatment
approaches
carefully
designed
either
inhibit
or
promote
ferroptosis.
Additionally,
succinctly
summarized
therapeutic
targets
compounds
that
hold
promise
targeting
within
various
facet
underscores
burgeoning
possibilities
manipulating
as
strategy.
summary,
enriched
insights
both
investigators
practitioners,
while
fostering
an
elevated
comprehension
latent
translational
utilities.
revealing
basic
processes
investigating
possibilities,
crucial
resource
scientists
medical
aiding
deep
understanding
effects
situations.
Frontiers in Cellular and Infection Microbiology,
Год журнала:
2023,
Номер
13
Опубликована: Март 3, 2023
Mycobacterium
tuberculosis
(Mtb),
the
causative
agent
of
Tuberculosis
(TB),
remains
a
pathogen
great
interest
on
global
scale.
This
airborne
affects
lungs,
where
it
interacts
with
macrophages.
Acidic
pH,
oxidative
and
nitrosative
stressors,
food
restrictions
make
macrophage’s
internal
milieu
unfriendly
to
foreign
bodies.
Mtb
subverts
host
immune
system
causes
infection
due
its
genetic
arsenal
secreted
effector
proteins.
In
vivo
in
vitro
research
have
examined
Mtb-host
macrophage
interaction.
interaction
is
crucial
stage
because
lung
macrophages
are
first
cells
encounters
host.
review
summarizes
effectors
that
interact
It
also
examines
how
control
eliminate
manipulates
defense
mechanisms
for
own
survival.
Understanding
these
TB
prevention,
diagnosis,
treatment.
Cell Death and Disease,
Год журнала:
2023,
Номер
14(10)
Опубликована: Окт. 23, 2023
Abstract
The
selenium-containing
enzyme
GPX4
moonlights
as
a
central
regulator
of
ferroptosis,
an
iron-dependent,
nonapoptotic
form
regulated
cell
death
caused
by
lipid
peroxidation.
Yet,
little
is
known
about
the
mechanisms
underlying
regulation
its
post-transcriptional
modifications.
Here,
we
identify
tripartite
motif-containing
protein
TRIM26
E3
ubiquitin
ligase
GPX4.
directly
interacts
with
through
Ring
domain
and
catalyzes
ubiquitination
at
K107
K117,
which
promotes
switch
in
polyubiquitination
from
K48
to
K63,
thus
enhancing
stability.
Moreover,
PLK1-mediated
S127
phosphorylation
enhances
interaction
between
Inhibition
causes
reduction
K63-linked
diminishes
levels
tumor
cells.
Further
investigation
revealed
that
overexpressed
glioma
silencing
dramatically
impedes
ferroptosis
resistance
tumorigenesis
vivo
vitro.
Clinically,
expression
shows
direct
correlation
PLK1
samples
associated
poor
outcome
patients
glioma.
Collectively,
these
findings
define
role
suggest
potential
strategy
for
treatment.
Pathogens,
Год журнала:
2023,
Номер
12(6), С. 839 - 839
Опубликована: Июнь 18, 2023
(Mtb)
modulates
diverse
cell
death
pathways
to
escape
the
host
immune
responses
and
favor
its
dissemination,
a
complex
process
of
interest
in
pathogenesis-related
studies.
The
main
virulence
factors
Mtb
that
alter
are
classified
according
their
origin
as
either
non-protein
(for
instance,
lipomannan)
or
protein
(such
PE
family
ESX
secretion
system).
38
kDa
lipoprotein,
ESAT-6
(early
antigen-secreted
6
kDa),
another
secreted
protein,
tuberculosis
necrotizing
toxin
(TNT),
induces
necroptosis,
thereby
allowing
mycobacteria
survive
inside
cell.
inhibition
pyroptosis
by
blocking
inflammasome
activation
Zmp1
PknF
is
pathway
aids
intracellular
replication
Mtb.
Autophagy
mechanism
allows
response.
enhanced
survival
(Eis)
other
proteins,
such
ESX-1,
SecA2,
SapM,
PE6,
certain
microRNAs,
also
facilitate
process.
In
summary,
affects
microenvironment
avoid
an
effective
response
spread.
A
thorough
study
these
would
help
identify
therapeutic
targets
prevent
host.
Journal of Advanced Research,
Год журнала:
2023,
Номер
54, С. 211 - 222
Опубликована: Янв. 23, 2023
Crush
syndrome
(CS)
is
a
kind
of
traumatic
and
ischemic
injury
that
seriously
threatens
life
after
prolonged
compression.
It
characterized
by
systemic
inflammatory
reaction,
myoglobinuria,
hyperkalemia
acute
kidney
(AKI).
Especially
AKI,
it
the
leading
cause
death
from
CS.
There
are
various
cell
forms
in
among
which
ferroptosis
typical
form
death.
However,
role
has
not
been
fully
revealed
CS-AKI.
This
review
aimed
to
summarize
evidence
CS-AKI
its
related
molecular
mechanism,
discuss
therapeutic
significance
CS-AKI,
open
up
new
ideas
for
treatment
One
main
pathological
manifestations
renal
tubular
epithelial
dysfunction
death,
attributed
massive
deposition
myoglobin.
Large
amounts
myoglobin
released
damaged
muscle
deposited
tubules,
impeding
normal
tubules
function
directly
damaging
with
oxidative
stress
elevated
iron
levels.
Lipid
peroxidation
damage
overload
distinguishing
features
ferroptosis.
Moreover,
high
levels
pro-inflammatory
cytokines
damage-associated
molecule
pattern
molecules
(HMGB1,
double-strand
DNA,
macrophage
extracellular
trap)
tissue
have
shown
promote
how
occurs
whether
can
be
target
remains
unclear.
In
our
current
work,
we
systematically
reviewed
occurrence
underlying
mechanism
Cell Death and Disease,
Год журнала:
2024,
Номер
15(11)
Опубликована: Ноя. 26, 2024
Abstract
Regulated
cell
death
(RCD)
refers
to
the
form
of
that
can
be
regulated
by
various
biomacromolecules.
Each
modalities
have
their
distinct
morphological
changes
and
molecular
mechanisms.
However,
intense
evidences
suggest
lipid
peroxidation
common
feature
initiates
propagates
death.
Excessive
alters
property
membrane
further
damage
proteins
nucleic
acids,
which
is
implicated
in
human
pathologies.
Here,
we
firstly
review
classical
chain
process
peroxidation,
clarify
current
understanding
myriad
roles
mechanisms
RCD
types.
We
also
discuss
how
involves
diseases
such
intimate
association
between
peroxidation-driven
leveraged
develop
rational
therapeutic
strategies.
