Nature Cardiovascular Research,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 24, 2025
Abstract
Myocarditis,
characterized
by
inflammatory
cell
infiltration,
can
have
multiple
etiologies,
including
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
infection
or,
rarely,
mRNA-based
disease
2019
(COVID-19)
vaccination.
The
underlying
cellular
and
molecular
mechanisms
remain
poorly
understood.
In
this
study,
we
performed
single-nucleus
RNA
sequencing
on
left
ventricular
endomyocardial
biopsies
from
patients
with
myocarditis
unrelated
to
COVID-19
(Non-COVID-19),
after
SARS-CoV-2
(Post-COVID-19)
vaccination
(Post-Vaccination).
We
identified
distinct
cytokine
expression
patterns,
interferon-γ
playing
a
key
role
in
Post-COVID-19,
upregulated
IL16
IL18
serving
as
hallmark
of
Post-Vaccination
myocarditis.
Although
myeloid
responses
were
similar
across
all
groups,
the
group
showed
higher
proportion
CD4
+
T
cells,
Post-COVID-19
exhibited
an
expansion
cytotoxic
CD8
natural
killer
cells.
Endothelial
cells
gene
changes
indicative
vascular
barrier
dysfunction
ongoing
angiogenesis
groups.
These
findings
highlight
shared
driving
without
history
or
EBioMedicine,
Journal Year:
2023,
Volume and Issue:
99, P. 104950 - 104950
Published: Dec. 30, 2023
Pulmonary
infection
with
SARS-CoV-2
stimulates
host
immune
responses
and
can
also
result
in
the
progression
of
dysregulated
critical
inflammation.
Throughout
pandemic,
management
treatment
COVID-19
has
been
continuously
updated
a
range
antiviral
drugs
immunomodulators.
Monotherapy
oral
antivirals
proven
to
be
effective
COVID-19.
However,
should
initiated
early
stages
ensure
beneficial
therapeutic
outcomes,
there
is
still
room
for
further
consideration
on
strategies
using
antivirals.
Phytomedicine Plus,
Journal Year:
2023,
Volume and Issue:
3(2), P. 100432 - 100432
Published: March 11, 2023
Schisandra
chinensis
fruit
is
a
well-known
traditional
Chinese
medicine
(TCM),
whose
extract
has
potent
inhibitory
effect
on
the
severe
acute
respiratory
syndrome-coronavirus-2
(SARS‑CoV‑2)
3-chymotrypsin-like
protease
(3CLpro)
and
papain-like
(PLpro).This
work
aims
to
find
active
components
from
of
S.
against
SARS‑CoV‑2
3CLpro
PLpro.The
chemical
constituents
were
retrieved
based
electronic
databases,
such
as
Web
Science,
PubMed,
Medline
Plus,
CNKI.
Molecular
docking
was
used
screen
PLpro.
Potential
hit
compounds
further
evaluated
by
enzymatic
activity
assay.
Furthermore,
anti-inflammatory
activities
explored
using
phorbol-12-myristate-13-acetate
(PMA)-induced
THP1
cells
model.In
this
work,
we
75
fruit,
including
62
dibenzocyclooctadiene-type
lignans,
3
diarylbutane-type
2
tetrahydrofuran-type
8
nortriterpenoids.
Combining
molecular
study
in
vitro
experiments,
found
that
pregomisin
(63),
meso‑dihydroguaiaretic
acid
(64),
nordihydroguaiaretic
(65)
could
potently
inhibit
with
IC50
values
3.07
±
0.38,
4.12
6.06
0.62
μM,
respectively,
PLpro
5.23
0.33,
4.24
0.46,
16.28
0.54
respectively.
Interestingly,
63,
64,
65
also
have
regulating
inflammatory
response
vitro.Our
results
suggest
may
be
promising
SARS-CoV-2
inhibitors
anti-inflammatory.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(6), P. 3463 - 3463
Published: March 19, 2024
In
COVID-19,
cytokine
release
syndrome
can
cause
severe
lung
tissue
damage
leading
to
acute
respiratory
distress
(ARDS).
Here,
we
address
the
effects
of
IFNγ,
TNFα,
IL-1β
and
IL-6
on
growth
arrest
alveolar
A549
cells,
focusing
role
IFN
regulatory
factor
1
(IRF1)
transcription
factor.
The
efficacy
JAK1/2
inhibitor
baricitinib
has
also
been
tested.
WT
IRF1
KO
cells
were
exposed
cytokines
for
up
72
h.
Cell
proliferation
death
evaluated
with
resazurin
assay,
analysis
cell
cycle
cycle-regulator
proteins,
LDH
Annexin-V
positivity;
induction
senescence
senescence-associated
secretory
phenotype
(SASP)
was
through
β-galactosidase
staining
quantitation
secreted
inflammatory
mediators.
While
IL-1
proved
ineffective,
IFNγ
plus
TNFα
caused
a
proliferative
in
alterations
morphology,
along
acquisition
phenotype.
These
STAT
IRF1-dependent
since
they
prevented
by
much
less
evident
than
cells.
STATs/IRF1
axis
is
required
cytokine-induced
Hence,
baricitininb
promising
therapeutic
strategy
attenuation
inflammation.
Nature Cardiovascular Research,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 24, 2025
Abstract
Myocarditis,
characterized
by
inflammatory
cell
infiltration,
can
have
multiple
etiologies,
including
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
infection
or,
rarely,
mRNA-based
disease
2019
(COVID-19)
vaccination.
The
underlying
cellular
and
molecular
mechanisms
remain
poorly
understood.
In
this
study,
we
performed
single-nucleus
RNA
sequencing
on
left
ventricular
endomyocardial
biopsies
from
patients
with
myocarditis
unrelated
to
COVID-19
(Non-COVID-19),
after
SARS-CoV-2
(Post-COVID-19)
vaccination
(Post-Vaccination).
We
identified
distinct
cytokine
expression
patterns,
interferon-γ
playing
a
key
role
in
Post-COVID-19,
upregulated
IL16
IL18
serving
as
hallmark
of
Post-Vaccination
myocarditis.
Although
myeloid
responses
were
similar
across
all
groups,
the
group
showed
higher
proportion
CD4
+
T
cells,
Post-COVID-19
exhibited
an
expansion
cytotoxic
CD8
natural
killer
cells.
Endothelial
cells
gene
changes
indicative
vascular
barrier
dysfunction
ongoing
angiogenesis
groups.
These
findings
highlight
shared
driving
without
history
or
