Cell Regeneration,
Journal Year:
2024,
Volume and Issue:
13(1)
Published: Nov. 27, 2024
Abstract
Macrophages
are
crucial
in
the
heart’s
development,
function,
and
injury.
As
part
of
innate
immune
system,
they
act
as
first
line
defense
during
cardiac
injury
repair.
After
events
such
myocardial
infarction
or
myocarditis,
numerous
macrophages
recruited
to
affected
areas
heart
clear
dead
cells
facilitate
tissue
This
review
summarizes
roles
resident
developing
cardiovascular
diseases.
We
also
describe
how
macrophage
phenotypes
dynamically
change
within
disease
microenvironment,
exhibiting
distinct
pro-inflammatory
anti-inflammatory
functions.
Recent
studies
reveal
values
targeting
diseases
treatment
novel
bioengineering
technologies
engineered
a
promising
therapeutic
strategy.
Engineered
have
strong
natural
tropism
infiltration
for
aiming
reduce
inflammatory
response,
inhibit
excessive
fibrosis,
restore
function
promote
regeneration.
discuss
recent
highlighting
strategies
new
approaches
macrophages,
which
can
aid
recovery.
Viruses,
Journal Year:
2025,
Volume and Issue:
17(3), P. 390 - 390
Published: March 10, 2025
Chronic
viral
infections
like
HIV,
HBV,
and
HCV
establish
persistent
interactions
with
the
host
immune
system,
resulting
in
evasion
long-term
dysfunction.
These
viruses
use
a
range
of
strategies
to
limit
defenses,
such
as
downregulating
MHC
class
I,
disrupting
interferon
signaling,
altering
apoptosis
pathways,
suppressing
cytotoxic
T-cell
activity.
Key
proteins,
including
HIV
Nef,
HBV
X
protein,
NS5A,
interfere
antigen
presentation
JAK/STAT
thereby
reducing
antiviral
responses.
induce
exhaustion
due
exposure,
which
leads
expression
inhibitory
receptors
PD-1
CTLA-4
on
T
cells.
Viral
epigenetic
changes,
N6-methyladenosine
modifications
histone
deacetylation,
enhance
by
modulating
gene
infected
Viruses
further
manipulate
cytokine
networks
promoting
an
immunosuppressive
environment
through
IL-10
TGF-β
secretion,
suppress
inflammatory
responses
inhibit
activation.
This
review
examines
molecular/cellular
mechanisms
that
enable
chronic
escape
immunity,
focusing
antigenic
variation,
disruption,
control
apoptotic
pathways.
It
also
addresses
how
genetic
factors,
HLA
polymorphisms,
influence
disease
progression.
Lastly,
we
discuss
host-targeted
therapies,
checkpoint
inhibitors,
treatments,
CRISPR.
Scandinavian Journal of Immunology,
Journal Year:
2025,
Volume and Issue:
101(4)
Published: April 1, 2025
Cardiovascular
diseases
(CVDs)
remain
a
leading
cause
of
global
mortality,
driven
by
risk
factors
such
as
dyslipidemia,
hypertension
and
diabetes.
Recent
research
has
highlighted
the
critical
role
inflammasomes,
particularly
NLRP3
inflammasome,
in
pathogenesis
various
CVDs,
including
hypertension,
atherosclerosis,
myocardial
infarction
heart
failure.
Inflammasomes
are
intracellular
protein
complexes
that
activate
inflammatory
responses
through
production
pro-inflammatory
cytokines
IL-1β
IL-18,
contributing
to
endothelial
dysfunction,
plaque
formation
injury.
This
review
provides
comprehensive
overview
structure,
activation
mechanisms
pathways
with
focus
on
their
involvement
cardiovascular
pathology.
Key
include
ion
fluxes
(K+
efflux
Ca2+
signalling),
endoplasmic
reticulum
(ER)
stress,
mitochondrial
dysfunction
lysosomal
destabilisation.
The
also
explores
therapeutic
potential
targeting
inflammasomes
mitigate
inflammation
improve
outcomes
CVDs.
Emerging
strategies
small-molecule
inhibitors,
biologics
RNA-based
therapeutics,
particular
emphasis
inhibition.
Additionally,
integration
artificial
intelligence
(AI)
offers
promising
avenues
for
identifying
novel
biomarkers,
predicting
disease
developing
personalised
treatment
strategies.
Future
directions
should
understanding
interactions
between
other
immune
components,
well
genetic
regulators,
uncover
new
targets.
By
elucidating
complex
this
underscores
innovative
therapies
address
inflammation-driven
pathology,
ultimately
improving
patient
outcomes.
Journal of Ovarian Research,
Journal Year:
2025,
Volume and Issue:
18(1)
Published: May 5, 2025
The
p53
tumor
suppressor
gene,
a
master
regulator
of
diverse
cellular
pathways,
is
frequently
altered
in
various
cancers.
Loss
function
genes
commonly
associated
with
the
onset/progression
cancer
and
treatment
resistance.
Currently,
approaches
for
restoration
TP53
expression,
including
small
molecules
DNA
therapies,
have
yielded
progressive
success,
but
each
has
formidable
drawbacks.
Here,
we
introduced
an
endogenous
nanoplatform
to
effectively
deliver
protein.
Briefly
speaking,
proteins
were
fused
by
Lamp2b
loaded
into
extracellular
vesicles-based
nanoparticles,
which
could
markedly
restore
expression
natural
TP53-deficient
ovarian
(OCs)
subsequently
inhibit
cell
proliferation
as
well
induce
apoptosis.
Moreover,
well-known
biotin
streptavidin
binding
strategy
was
used
confer
targeting
ability.
Since
mesothelin
(MSLN)
expressed
highly
cancer,
anti-MSLN
engineered
MSLN
exert
anti-tumor
Our
findings
indicated
that
suppressors
be
promising
nanotechnology
potential
treatment.
Nanoscale,
Journal Year:
2024,
Volume and Issue:
16(16), P. 7825 - 7840
Published: Jan. 1, 2024
This
review
introduces
the
modified
methods
of
engineered
EVs,
summarizes
application
EVs
in
preclinical
and
clinical
trials,
discusses
opportunities
challenges
for
translation
surface-engineered
EVs.
Extracellular Vesicles and Circulating Nucleic Acids,
Journal Year:
2024,
Volume and Issue:
5(3), P. 458 - 60
Published: July 7, 2024
Extracellular
vesicles
(EVs)
are
increasingly
acknowledged
as
important
mediators
of
intercellular
communication,
closely
related
to
the
occurrence
and
development
a
variety
diseases.
Numerous
studies
have
demonstrated
that
EVs
play
multifaceted
role
in
infection
process
viral
diseases,
elucidating
their
ability
both
facilitate
spread
inhibit
progression.
These
versatile
entities
not
only
enhance
rates
widen
scope
through
transmission
entire
viruses
or
genomes,
but
also
trigger
antiviral
responses
prompt
cytokine
secretion
near
site,
thereby
fortifying
host's
defense
mechanisms
safeguarding
neighboring
cells
against
infection.
This
complicated
crosstalk
between
infections
prompts
deeper
exploration
into
roles
potential
clinical
applications.
In
this
review,
we
aim
encapsulate
recent
advances
understanding
intricate
interplay
EVs,
shedding
light
on
underlying
vesicle-to-virion
crosstalk.
Furthermore,
underscore
significance
harnessing
knowledge
for
diagnostic
therapeutic
functions
combating
Research Square (Research Square),
Journal Year:
2024,
Volume and Issue:
unknown
Published: Dec. 23, 2024
Abstract
Group
2
innate
lymphoid
cells
(ILC2s)
promote
the
recruitment
of
eosinophils
by
secreting
large
amounts
type
cytokines
(IL-5
and
IL-13),
thus
triggering
main
feature
asthma,
pathological
inflammation.
Recent
insights
from
mouse
human
studies
indicated
a
potential
relationship
between
ILC2s
macrophages.
However,
mechanism
which
lung
M2
macrophage-derived
extracellular
vesicles
(M2
EVs)
regulate
remains
unclear.
Here,
size,
morphology,
specific
markers
EVs
were
successfully
characterized
in
lungs.
Furthermore,
we
discovered
that
strongly
promoted
immunopathology
induced
papain.
Mechanistically,
internalized
ILC2s,
ILC2
activation
inducing
pro-inflammatory
cytokine
IL-13)
production.
also
indirectly
enhanced
function
through
macrophages
CD4+
T
cells.
Using
RNA
sequencing,
found
long
non-coding
(lncRNA)
4930474H06Rik
participated
mediating
these
effects
EVs.
Inhibition
altered
intracellular
metabolism
activated
NF-κB
pathway
signaling.
Taken
together,
demonstrated
allergic
airway
inflammation
at
least
partially
4930474H06Rik,
implying
can
be
considered
as
therapeutic
target
for
Cell Regeneration,
Journal Year:
2024,
Volume and Issue:
13(1)
Published: Nov. 27, 2024
Abstract
Macrophages
are
crucial
in
the
heart’s
development,
function,
and
injury.
As
part
of
innate
immune
system,
they
act
as
first
line
defense
during
cardiac
injury
repair.
After
events
such
myocardial
infarction
or
myocarditis,
numerous
macrophages
recruited
to
affected
areas
heart
clear
dead
cells
facilitate
tissue
This
review
summarizes
roles
resident
developing
cardiovascular
diseases.
We
also
describe
how
macrophage
phenotypes
dynamically
change
within
disease
microenvironment,
exhibiting
distinct
pro-inflammatory
anti-inflammatory
functions.
Recent
studies
reveal
values
targeting
diseases
treatment
novel
bioengineering
technologies
engineered
a
promising
therapeutic
strategy.
Engineered
have
strong
natural
tropism
infiltration
for
aiming
reduce
inflammatory
response,
inhibit
excessive
fibrosis,
restore
function
promote
regeneration.
discuss
recent
highlighting
strategies
new
approaches
macrophages,
which
can
aid
recovery.
