Cardiology in Review,
Год журнала:
2024,
Номер
unknown
Опубликована: Янв. 29, 2024
Long
coronavirus
disease
(COVID)
is
the
development
or
persistence
of
symptoms
after
an
acute
SARS-CoV-2
(COVID-19)
infection.
Fewer
patients
are
developing
COVID-19
infections,
but
with
long
COVID
continue
to
have
alarming
long-term
sequelae.
Many
cardiac
magnetic
resonance
imaging
studies
show
significant
changes
in
structure
a
infection,
suggestive
increased
burden
many
cardiovascular
diseases,
notably
myocarditis.
The
pathophysiology
requires
viral
binding
angiotensin-converting
enzyme
2
protein
receptors
throughout
body,
which
upregulated
by
inflammation.
Consequently,
numerous
preexisting
conditions
that
worsen
prolong
inflammation
enhance
this
and
differing
effects
on
based
their
unique
immune
systems.
These
pathophysiological
drive
sequelae
such
as
inappropriate
sinus
tachycardia,
postural
orthostatic
other
types
intolerance.
Increased
screening
for
low-risk
interventions
exercise
regimens
could
alleviate
suffering
endured
COVID.
Researching
Enhance
Recovery
Initiative
(RECOVER)
trials
at
National
Institutes
Health
exploring
potential
treatments
patients.
“All
diseases
originate
in
the
gut.”
Hippocrates
(400
BC)
A
healthy
gut
microbiome
via
gut-brain-axis
elevates
heart
rate
variability
(HRV),
a
general
measure
of
health
and
well-being.
dysbiotic
microbiome,
low
biodiversity
butyrate
producers,
can
alter
tryptophan
metabolism
(ATM)
increase
kynurenine
to
ratio
(KTR)
with
release
proinflammatory
cytokines,
predominantly
TNF-α,
IL-6,
IL-1β.
These
also
characterize
chronic
inflammation,
oxidative
stress,
multitude
diseases.
Also
proposed
is
gut-lung
dysbiosis
concept
consequent
degradation
ACE2
(richest
lungs
gut).
Leaky
(and
lung)
induced
autoantibodies
(AAs)
related
G-protein
coupled
receptors
(GPCRs)
combination
increased
Ang
II
further
potentiate
stress.
The
underappreciated
pathogenic
role
these
on
invading
Candida
hyphae
explored.
efficacy
fecal
transplantation
(FMT)
treating
dementia,
cancer,
autoimmunity
supports
plausibility
success
“FMT-lite”.
This
triple
play
prebiotic
(d-mannose),
probiotic
(bifidobacteria
lactobacilli),
postbiotic
(butyrate)
might
improve
intestinal
barrier
integrity,
oppose
entry
GPCR
antigens
(epitopes),
suppress
inflammatory
cytokine
triad,
balance
IFN-γ
TGF-β,
depress
KTR,
elevate
HRV,
extend
lifespan
its
quality.
npj Systems Biology and Applications,
Год журнала:
2025,
Номер
11(1)
Опубликована: Янв. 13, 2025
Coronavirus
disease
2019
(COVID-19)
presents
a
wide
spectrum
of
symptoms,
the
causes
which
remain
poorly
understood.
This
study
explored
associations
between
autoantibodies
(AABs),
particularly
those
targeting
G
protein-coupled
receptors
(GPCRs)
and
renin‒angiotensin
system
(RAS)
molecules,
clinical
manifestations
COVID-19.
Using
cross-sectional
analysis
244
individuals,
we
applied
multivariate
variance,
principal
component
analysis,
multinomial
regression
to
examine
relationships
AAB
levels
key
symptoms.
Significant
correlations
were
identified
specific
AABs
symptoms
such
as
fever,
muscle
aches,
anosmia,
dysgeusia.
Notably,
anti-AGTR1
antibodies,
contribute
endothelial
glycocalyx
(eGC)
degradation,
process
reversed
by
losartan,
have
emerged
strong
predictors
core
increased
with
symptom
accumulation,
peaking
in
patients
exhibiting
all
four
These
findings
highlight
role
AABs,
determining
severity
suggest
their
involvement
pathophysiology
COVID-19,
including
vascular
complications.
Clinical Immunology,
Год журнала:
2025,
Номер
unknown, С. 110454 - 110454
Опубликована: Фев. 1, 2025
Here,
we
investigate
how
autoantibodies
against
G
protein-coupled
receptors
(GPCRs)
on
endothelial
cells,
which
are
present
in
patients
with
scleroderma
renal
crisis
(SRC)
impact
endothelin-1
(ET-1)
production
human
microvascular
cells
(HMECs).
To
this
end,
serum
IgG
fraction
was
isolated
from
SRC
and
applied
to
HMECs
culture.
Compared
treated
either
plain
control
medium
or
healthy
individuals,
exposure
of
SRC-IgG
resulted
a
time-
concentration-dependent
increase
ET-1
expression
release.
This
effect
could
be
blocked
by
the
protease
activated
receptor
1
(PAR1)
inhibitor
mimicked
thrombin,
PAR1
activator.
Transcription
factor
C-FOS/AP-1
tissue
(TF)
were
identified
as
mediators
these
responses.
Thus,
it
can
concluded
that
stimulates
produce
ET-1,
acting
through
cooperation
TF.
Current Opinion in Rheumatology,
Год журнала:
2023,
Номер
35(6), С. 309 - 316
Опубликована: Июль 24, 2023
Purpose
of
review
In
patients
with
systemic
sclerosis
(SSc),
vascular
manifestations
precede
skin
and
organ
fibrosis.
There
is
increasing
evidence
demonstrating
a
pathogenic
link
between
early
injury
subsequent
development
tissue
Recent
findings
Our
knowledge
cellular
molecular
mechanisms
underlying
unique
relationship
SSc-related
vasculopathy
fibrosis
has
changed
over
the
last
few
years.
showing
viral
infection
as
potential
trigger
elucidating
injury.
Due
to
defective
repair
machinery,
this
initial
event
results
in
endothelial
cell
activation
apoptosis
well
recruitment
inflammatory/immune
cells,
leading
endothelial-to-mesenchymal
transition.
This
sequential
process
induces
destructive
capillaries,
fibroproliferative
lesions
arteries,
excessive
surrounding
tissue.
A
variety
pathways
involved
remodeling
linked
have
been
identified
serve
attractive
therapeutic
targets
for
SSc.
Summary
Endothelial
may
play
central
role
connecting
three
features
that
characterize
SSc
pathogenesis:
vasculopathy,
chronic
inflammation,
understanding
processes
responsible
myofibroblast
differentiation
triggered
by
will
provide
rationale
novel
targeted
therapies
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(4), С. 2299 - 2299
Опубликована: Фев. 15, 2024
Systemic
sclerosis
(SSc)
is
a
multifaceted
connective
tissue
disease
whose
aetiology
remains
largely
unknown.
Autoimmunity
thought
to
play
pivotal
role
in
the
development
of
disease,
but
direct
pathogenic
SSc-specific
autoantibodies
be
established.
The
recent
discovery
functional
antibodies
targeting
G-protein-coupled
receptors
(GPCRs),
presence
has
been
demonstrated
different
autoimmune
conditions,
shed
some
light
on
SSc
pathogenesis.
These
bind
GPCRs
expressed
immune
and
non-immune
cells
as
their
endogenous
ligands,
exerting
either
stimulatory
or
inhibitory
effect
corresponding
intracellular
pathways.
Growing
evidence
suggests
that,
SSc,
anti-GPCRs
correlates
with
specific
clinical
manifestations.
Autoantibodies
endothelin
receptor
type
A
(ETAR)
angiotensin
1
(AT1R)
are
associated
severe
vasculopathic
SSc-related
manifestations,
while
anti-C-X-C
motif
chemokine
(CXCR)
seem
predictive
interstitial
lung
involvement;
anti-muscarinic-3
acetylcholine
(M3R)
have
found
patients
gastrointestinal
involvement
anti-protease-activated
(PAR1)
detected
experiencing
scleroderma
renal
crisis.
This
review
aims
clarify
potential
pathogenetic
significance
GPCR-targeting
focusing
associations
manifestations
scleroderma.
An
extensive
examination
autoimmunity
might
provide
valuable
insights
into
underlying
mechanisms
thus
enabling
novel
therapeutic
strategies
tailored
target
GPCR-mediated
