Animals,
Год журнала:
2024,
Номер
14(23), С. 3516 - 3516
Опубликована: Дек. 5, 2024
Epidemic
encephalitis
B
caused
by
Japanese
virus
(JEV)
is
a
common
zoonotic
disease
that
poses
threats
to
both
pigs
and
humans.
The
cellular
defense
mechanism
closely
tied
the
body's
resistance
viral
invasion.
Regulated
cell
death,
such
as
ferroptosis,
strategy
employed
host
cells
defend
against
invasions.
To
understand
effect
of
ferroptosis
on
proliferation
JEV,
experimentally
infected
PK15
were
treated
with
agonist
or
antagonist.
results
indicated
can
suppress
JEV
proliferation,
whereas
antagonist
promotes
proliferation.
Functional
enrichment
analysis
showed
Erastin
SP600125
could
affect
through
TNF,
IL-17,
Toll-like
receptor,
PI3K-AKT,
chemokine
signaling
pathways,
well
ECM-receptor
interactions.
Combined
transcriptome
proteome
analyses
revealed
31
important
genes,
which
are
significantly
associated
inflammatory
response.
Our
provide
better
understanding
molecular
mechanisms
affects
JEV.
Cancers,
Год журнала:
2025,
Номер
17(3), С. 530 - 530
Опубликована: Фев. 5, 2025
Background:
Despite
advances
in
the
management
of
head
and
neck
squamous
cell
carcinoma
(HNSCC),
prognostic
models
treatment
strategies
remain
inadequate,
particularly
for
HPV-positive
oropharyngeal
(OPSCC).
The
rising
incidence
OPSCC
highlights
an
urgent
need
innovative
therapeutic
approaches.
Ferroptosis,
a
regulated
form
non-apoptotic
death,
has
gained
attention
its
role
cancer
progression,
but
potential
as
target
remains
largely
unexplored.
This
study
investigates
ferroptosis
OPSCC,
aiming
to
identify
markers
provide
insights
into
that
could
improve
patient
outcomes.
Methods:
Thirteen
gene
expression
signatures
were
retrieved
from
literature,
their
performance
association
immune
microenvironment
validated
on
meta-analysis
267
cases
(Metanalysis-HPV267)
286
samples
BD2Decide
project
(BD2-HPV286).
Results:
Our
analysis
revealed
specific
ferroptosis-related
signatures,
FER3,
FER4,
FER6,
FER12,
are
significantly
associated
(p-value
<
0.05)
with
high-risk
groups
adverse
tumor
features,
including
suppressed
activity
enhanced
stromal
involvement.
Elevated
CAV1,
suppressor,
further
delineates
profiles.
Conclusions:
These
findings
highlight
significance
stratifying
patients
identifying
those
poorer
clinical
Targeting
pathways
represents
novel
promising
approach
addressing
unmet
effective
OPSCC.
Future
research
should
focus
translating
these
applications
advance
precision
oncology
outcomes
this
growing
population.
The Journal of Steroid Biochemistry and Molecular Biology,
Год журнала:
2025,
Номер
249, С. 106710 - 106710
Опубликована: Фев. 20, 2025
The
interaction
between
vitamin
D
and
the
immune
system
is
perhaps
most
well
recognised
extraskeletal
facet
of
D,
encompassing
early
studies
therapy
for
TB
leprosy
through
to
more
recent
links
with
autoimmune
disease.
However,
spotlight
on
function
has
been
particularly
intense
in
last
five
years
following
COVID-19
pandemic.
This
was
due,
part,
many
association
status
infection
disease
prognosis,
as
smaller
number
clinical
trials
supplementation.
a
potential
role
also
stemmed
from
basic
biology
that
provides
plausible
mechanistic
rationale
beneficial
effects
improved
health
setting
respiratory
infection.
aim
this
review
summarise
different
strands
evidence
supporting
effect
COVID-19,
how
modified
during
pandemic
itself,
new
aspects
are
likely
arise
near
future.
Key
topics
feature
are:
antibacterial
versus
antiviral
innate
responses
1,25-dihydroxyvitamin
(1,25(OH)2D);
1α-hydroxylase
(CYP27B1)
activity
metabolism
25-hydroxyvitamin
(25(OH)D)
beyond
antigen-presenting
cells;
advances
cell
target
gene
(notably
changes
metabolic
profile).
Whilst
much
interest
era
focused
public
health,
continued
evolution
our
understanding
interacts
components
continues
support
health.
Cells,
Год журнала:
2025,
Номер
14(5), С. 351 - 351
Опубликована: Фев. 28, 2025
Human
immunodeficiency
virus
(HIV)
infection
continues
to
be
a
major
global
health
challenge,
affecting
38.4
million
according
the
Joint
United
Nations
Program
on
HIV/AIDS
(UNAIDS)
at
end
of
2021
with
1.5
new
infections.
New
HIV
infections
increased
during
2
years
after
COVID-19
pandemic.
Understanding
intricate
cellular
processes
underlying
pathogenesis
is
crucial
for
developing
effective
therapeutic
strategies.
Among
these
processes,
autophagy
and
programmed
cell
death
modalities,
including
apoptosis,
necroptosis,
pyroptosis,
ferroptosis,
play
pivotal
roles
in
host-virus
interaction
dynamics.
Autophagy,
highly
conserved
mechanism,
acts
as
double-edged
sword
infection,
influencing
viral
replication,
immune
response
modulation,
fate
infected
cells.
Conversely,
critical
defense
mechanism
against
spread
contributes
depletion
CD4+
T
cells,
hallmark
progression.
This
review
aims
dissect
complex
interplay
between
modalities
HIV-induced
pathogenesis.
It
highlights
molecular
mechanisms
involved,
their
persistence
dysfunction,
challenges
posed
by
reservoir
drug
resistance,
which
continue
impede
management
pathology.
Targeting
pathways
holds
promise
novel
strategies
mitigate
chronic
inflammation,
ultimately
improving
outcomes
individuals
living
HIV.
Biomedicine & Pharmacotherapy,
Год журнала:
2024,
Номер
176, С. 116866 - 116866
Опубликована: Июнь 14, 2024
Enterovirus
71
(EV71),
a
prominent
pathogen
associated
with
hand,
foot,
and
mouth
disease
(HFMD),
has
been
reported
worldwide.
To
date,
the
advancement
of
effective
drugs
targeting
EV71
remains
in
preliminary
experimental
stage.
In
this
study,
magnolol
demonstrated
significant
dose-dependent
inhibition
replication
vitro.
It
upregulated
overall
expression
level
nuclear
factor
erythroid
2
-
related
(Nrf2)
facilitated
its
nucleus
translocation,
resulting
increased
various
ferroptosis
inhibitory
genes.
This
process
led
to
reduction
reactive
oxygen
species
(ROS)
accumulation
induced
by
viral
infection.
Additionally,
exhibited
broad-spectrum
antiviral
effect
against
enteroviruses.
Notably,
treatment
substantially
enhanced
survival
rate
EV71-infected
mice,
attenuated
load
heart,
liver,
brain,
limb
tissues,
mitigated
tissue
inflammation.
Taken
together,
emerges
as
promising
candidate
for
development
anti-EV71
drugs.
Military Medical Research,
Год журнала:
2024,
Номер
11(1)
Опубликована: Дек. 16, 2024
Abstract
Sepsis,
characterized
as
life-threatening
organ
dysfunction
resulting
from
dysregulated
host
responses
to
infection,
remains
a
significant
challenge
in
clinical
practice.
Despite
advancements
understanding
host-bacterial
interactions,
molecular
responses,
and
therapeutic
approaches,
the
mortality
rate
associated
with
sepsis
has
consistently
ranged
between
10
16%.
This
elevated
highlights
critical
gaps
our
comprehension
of
etiology.
Traditionally
linked
bacterial
fungal
pathogens,
recent
outbreaks
acute
viral
infections,
including
Middle
East
respiratory
syndrome
coronavirus
(MERS-CoV),
influenza
virus,
severe
2
(SARS-CoV-2),
among
other
regional
epidemics,
have
underscored
role
pathogenesis
sepsis,
particularly
when
critically
ill
patients
exhibit
classic
symptoms
indicative
sepsis.
However,
many
cases
viral-induced
are
frequently
underdiagnosed
because
standard
evaluations
typically
exclude
panels.
Moreover,
these
viruses
not
only
activate
conventional
pattern
recognition
receptors
(PRRs)
retinoic
acid-inducible
gene-I
(RIG-I)-like
(RLRs)
but
also
initiate
primary
antiviral
pathways
such
cyclic
guanosine
monophosphate
adenosine
(GMP-AMP)
synthase
(cGAS)-stimulator
interferon
genes
(STING)
signaling
response
mechanisms.
Such
activations
lead
cellular
stress,
metabolic
disturbances,
extensive
cell
damage
that
exacerbate
tissue
injury
while
leading
spectrum
manifestations.
complexity
poses
substantial
challenges
for
management
affected
cases.
In
this
review,
we
elucidate
definition
diagnosis
criteria
synthesizing
current
knowledge
regarding
its
etiology,
epidemiology,
pathophysiology,
mechanisms
involved
therein
well
their
impact
on
immune-mediated
damage.
Additionally,
discuss
considerations
related
both
existing
therapies
advanced
treatment
interventions,
aiming
enhance
comprehensive
surrounding
Journal of Virology,
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 8, 2025
ABSTRACT
Peste
des
petits
ruminants
virus
(PPRV)
is
an
important
pathogen
that
seriously
affects
the
productivity
of
small
worldwide.
Ferroptosis
a
programmed
cell
death
characterized
by
iron-dependent
lipid
peroxidation
and
accumulation
reactive
oxygen
species
(ROS).
Emerging
evidence
has
demonstrated
mitochondria
play
diverse
roles
in
process
ferroptosis,
but
interaction
between
ferroptosis
during
infection
remains
largely
unknown.
Here,
we
demonstrate
PPRV
induces
including
Fe
2+
overload,
peroxidation,
shrinkage
mitochondria.
Importantly,
crucial
role
PPRV-induced
decreased
mitochondrial
GPX4
Mechanistically,
downregulates
Lon
protease-1
(LONP1)
expression,
multifaceted
enzyme
essential
for
maintaining
homeostasis
function,
which
leads
to
degradation
through
Nrf2/Keap
pathway
ROS
More
importantly,
tightly
associated
with
inflammatory
responses
enhanced
replication.
Overall,
this
study
first
show
LONP1-mediated
involved
infection.
IMPORTANCE
transient
severe
immunosuppression
host,
threatens
both
livestock
endangered
susceptible
wildlife
populations
many
countries.
Despite
extensive
research,
it
unknown
whether
causes
what
mechanism
regulation
is.
Our
data
provide
direct
relationship
(LONP1)-mediated
dysfunctional
consequent
induction
pathogenesis.
via
mitochondria,
replication
levels.
Taken
together,
our
research
provided
new
insight
into
understanding
effect
on
pathogenesis
revealed
potential
therapeutic
target
antiviral
intervention.
Journal of Zhejiang University (Medical Sciences),
Год журнала:
2025,
Номер
unknown
Опубликована: Май 1, 2025
Paramyxoviruses
are
significant
respiratory
pathogens
with
substantial
clinical
relevance
in
pediatric
infectious
diseases.
During
infection,
they
induce
multiple
forms
of
programmed
cell
death
(PCD),
which
play
pivotal
roles
viral
replication,
dissemination,
and
host
immune
responses,
thereby
profoundly
influencing
the
life
cycle
disease
progression.
On
one
hand,
PCD
facilitates
clearance
infected
cells,
restricts
spread,
activates
defenses,
enhancing
antiviral
immunity.
other
excessive
or
dysregulated
may
lead
to
tissue
damage
imbalance,
creating
a
microenvironment
conducive
replication
exacerbating
severity.
For
instance,
apoptosis-mediated
by
both
intrinsic
extrinsic
pathways-contributes
infection
control
but
also
be
hijacked
viruses
promote
dissemination.
Pyroptosis,
driven
inflammasome
activation,
triggers
lytic
release
pro-inflammatory
cytokines.
Necroptosis,
mediated
RIPK1-RIPK3-MLKL
signaling
axis,
pyroptosis
amplify
innate
responses
concurrently
inflammatory
dysregulation.
Immunogenic
(ICD),
characterized
damage-associated
molecular
patterns
(DAMPs)
neoantigens,
antigen-specific
holds
therapeutic
potential
for
antitumor
interventions.
Emerging
evidence
suggests
that
ferroptosis,
through
modulation
iron
metabolism
associated
transporters,
participate
clearance.
This
review
comprehensively
summarizes
apoptosis,
pyroptosis,
necroptosis,
ICD,
ferroptosis
paramyxovirus
aiming
deepen
understanding
pathogenesis
provide
insights
developing
novel
strategies,
particularly
populations.