Abstract
Mycobacterium
tuberculosis
(
M.
tb
)
is
a
significant
intracellular
pathogen
responsible
for
numerous
infectious
disease‐related
deaths
worldwide.
It
uses
ESX‐1
T7SS
to
damage
phagosomes
and
enter
the
cytosol
of
host
cells
after
phagocytosis.
During
infection,
mitochondria
release
dsDNA,
which
activates
CGAS‐STING1
pathway.
This
pathway
leads
production
type
I
interferons
proinflammatory
cytokines
autophagy,
targets
degrades
bacteria
within
autophagosomes.
However,
role
IFNs
in
immunity
against
controversial.
While
previous
research
has
suggested
protective
role,
recent
findings
from
cgas‐sting1
knockout
mouse
studies
have
contradicted
this.
Additionally,
study
using
mice
non‐human
primate
models
uncovered
new
mechanism
by
neutrophils
recruited
lung
infections
form
neutrophil
extracellular
traps.
Activating
plasmacytoid
dendritic
causes
them
produce
IFNs,
interfere
with
function
interstitial
macrophages
increase
likelihood
tuberculosis.
Notably,
its
virulence
proteins
disrupt
signaling
leading
enhanced
pathogenesis.
Investigating
can
help
develop
ways
fight
In
the
realm
of
cancer
research,
tumor
microenvironment
(TME)
plays
a
crucial
role
in
initiation
and
progression,
shaped
by
complex
interactions
between
cells
surrounding
non-cancerous
cells.
Cytokines,
as
essential
immunomodulatory
agents,
are
secreted
various
cellular
constituents
within
TME,
including
immune
cells,
cancer-associated
fibroblasts,
themselves.
These
cytokines
facilitate
intricate
communication
networks
that
significantly
influence
initiation,
metastasis,
suppression.
Pyroptosis
contributes
to
TME
remodeling
promoting
release
pro-inflammatory
sustaining
chronic
inflammation,
impacting
processes
such
escape
angiogenesis.
However,
challenges
remain
due
interplay
among
cytokines,
pyroptosis,
along
with
dual
effects
pyroptosis
on
progression
therapy-related
complications
like
cytokine
syndrome.
Unraveling
these
complexities
could
strategies
balance
inflammatory
responses
while
minimizing
tissue
damage
during
therapy.
This
review
delves
into
crosstalk
elucidating
their
contribution
metastasis.
By
synthesizing
emerging
therapeutic
targets
innovative
technologies
concerning
this
aims
provide
novel
insights
enhance
treatment
outcomes
for
patients.
Journal of Inflammation Research,
Год журнала:
2024,
Номер
Volume 17, С. 7819 - 7835
Опубликована: Окт. 1, 2024
Sepsis
is
a
common
critical
illness
characterized
by
high
mortality
rates
and
significant
disease
burden.
In
the
context
of
sepsis-induced
organ
dysfunction,
lungs
are
among
initial
organs
affected,
which
may
progress
to
acute
lung
injury
(ALI)
respiratory
distress
syndrome
(ARDS).
Recent
studies
have
highlighted
crucial
roles
mitophagy
ferroptosis
in
development
progression
ALI/ARDS.
Identifying
key
convergence
points
these
processes
provide
valuable
insights
for
treatment
this
condition.
recent
years,
certain
herbs
their
bioactive
compounds
demonstrated
unique
benefits
managing
ALI/ARDS
modulating
or
ferroptosis.
This
review
summary
mechanisms
ferroptosis,
explores
interactions,
emphasizes
regulatory
Additionally,
it
offers
novel
perspective
on
strategies
summarizing
various
relevant
Frontiers in Cell Death,
Год журнала:
2025,
Номер
3
Опубликована: Янв. 7, 2025
Pyroptosis
is
a
form
of
proinflammatory
cell
death
characterized
by
inflammasome
activation,
pore
formation,
and
the
release
pro-inflammatory
cytokines
such
as
interleukin-1β
(IL-1β)
IL-18
upon
rupture.
Nuclear
factor-κB
(NF-κB),
prototypical
transcription
factor,
plays
critical
role
in
immune
system
regulation.
Recent
research
highlights
multifaceted
roles
NF-κB
signaling
pyroptosis.
Various
immunologically
relevant
ligands
their
receptors
can
activate
pathway
to
promote
pyroptosis,
with
Toll-like
(TLRs),
IL-1
(IL-1Rs),
TNF
(TNFRs)
being
most
prominent.
regulates
key
components
inflammasomes
involved
particularly
NLRP3
inflammasome.
studies
also
indicate
that
modulates
activation
NLRC4
AIM2
through
distinct
pathways
diverse
inflammatory
conditions,
acute
lung
injury
neuroinflammation.
Additionally,
mediates
production
cytokines,
including
IL-1β,
IL-33,
TNF-α,
which
further
regulate
This
review
examines
recent
advances
understanding
regulating
pyroptosis
during
infection
inflammation.
Clinical and Experimental Neuroimmunology,
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 17, 2025
Abstract
Parkinson's
disease
(PD)
is
a
progressive
neurodegenerative
disorder
characterized
by
the
loss
of
dopaminergic
neurons
in
substantia
nigra
pars
compacta,
leading
to
hallmark
motor
symptoms
such
as
bradykinesia,
tremors,
and
rigidity.
Emerging
evidence
suggests
that
dysregulation
or
aberrant
expression
long
noncoding
RNAs
(lncRNAs)
plays
critical
role
pathogenesis
PD
activating
inflammasome,
either
directly
via
oxidative
stress.
Aberrant
lncRNA
has
been
linked
alterations
genes
related
stress,
causing
an
imbalance
between
reactive
oxygen
species
(ROS)
antioxidant
defenses.
This
contributes
mitochondrial
dysfunction
neuronal
damage.
The
NLRP3
inflammasome
multiprotein
complex
comprising
sensor
protein
(eg,
NLRP3),
adaptor
(ASC),
effector
(caspase‐1).
Its
activation
involves
priming
NF‐κB
signaling
triggered
ROS,
dysfunction,
death‐associated
molecular
patterns,
extracellular
ATP.
Once
activated,
promotes
cleavage
maturation
proinflammatory
cytokines
IL‐1β
IL‐18,
amplifying
neuroinflammation
neurodegeneration
PD.
Crosstalk
dysregulated
lncRNAs,
ROS
production,
creates
vicious
cycle
neurodegeneration,
exacerbating
progression.
review
explores
mechanisms
linking
PD,
through
It
also
highlights
key
lncRNAs
involved
these
processes.
Furthermore,
potential
therapeutic
strategies
targeting
pathways,
antioxidants,
modulators,
inhibitors,
offer
promising
avenues
mitigate
slow
World Journal of Gastrointestinal Oncology,
Год журнала:
2025,
Номер
17(2)
Опубликована: Янв. 18, 2025
Hepatocellular
carcinoma
(HCC)
ranks
as
the
fourth
leading
cause
of
cancer-related
deaths
in
China,
and
treatment
options
are
limited.
The
cyclic
guanosine
monophosphate-adenosine
monophosphate
synthase
(cGAS)
activates
stimulator
interferon
gene
(STING)
signaling
pathway
a
crucial
immune
response
cytoplasm,
which
detects
cytoplasmic
DNA
to
regulate
innate
adaptive
responses.
As
potential
therapeutic
target,
cGAS-STING
markedly
inhibits
tumor
cell
proliferation
metastasis,
with
its
activation
being
particularly
relevant
HCC.
However,
prolonged
may
lead
an
immunosuppressive
microenvironment,
fostering
invasion
or
metastasis
liver
cells.
To
investigate
dual-regulation
mechanism
This
review
was
conducted
according
PRISMA
guidelines.
study
comprehensive
search
for
articles
related
HCC
on
PubMed
Web
Science
databases.
Through
rigorous
screening
meticulous
analysis
retrieved
literature,
research
aimed
summarize
elucidate
impact
tumors.
All
authors
collaboratively
selected
studies
inclusion,
extracted
data,
initial
online
databases
yielded
1445
studies.
After
removing
duplicates,
remaining
964
records
were
screened.
Ultimately,
55
met
inclusion
criteria
included
this
review.
Acute
inflammation
can
have
few
inhibitory
effects
cancer,
while
chronic
generally
promotes
progression.
Extended
will
result
suppressive
microenvironment.
Sclerosis,
Год журнала:
2025,
Номер
3(1), С. 6 - 6
Опубликована: Фев. 3, 2025
Apolipoprotein
L1
(APOL1)
genetic
variations,
notably
the
G1
and
G2
alleles,
have
important
roles
in
pathophysiology
of
focal
segmental
glomerulosclerosis
(FSGS)
other
kidney
problems,
especially
people
African
descent.
This
review
summarizes
current
understanding
about
genetic,
molecular,
clinical
features
APOL1-associated
FSGS
investigates
new
therapeutic
options.
It
reveals
how
APOL1
mutations
generate
injury
through
mechanisms
such
as
podocyte
dysfunction,
mitochondrial
impairment,
dysregulated
inflammatory
networks.
Recent
treatment
developments,
small-molecule
inhibitors
like
inaxaplin,
antisense
oligonucleotides,
novel
interventions
targeting
lipid
metabolism
pathways,
are
being
assessed
for
their
capacity
to
address
specific
issues
presented
by
nephropathy.
We
also
gaps
knowledge,
function
environmental
triggers
systemic
consequences
mutations,
emphasizing
significance
targeted
research.
