Pulmonary Circulation,
Journal Year:
2024,
Volume and Issue:
14(4)
Published: Oct. 1, 2024
Abstract
Leveraging
the
potential
of
virtual
platforms
in
post‐COVID‐19
era,
Infection
and
Pulmonary
Vascular
Diseases
Consortium
(iPVDc),
with
support
Research
Institute
(PVRI),
launched
a
globally
accessible
educational
program
to
highlight
top‐notch
research
on
inflammation
infectious
diseases
affecting
lung
vasculature.
This
innovative
series
has
already
successfully
brought
together
distinguished
investigators
across
five
continents
–
Asia,
Europe,
South
North
America,
Africa.
Moreover,
these
open
global
forums
have
contributed
comprehensive
understanding
complex
interplay
among
immunology,
inflammation,
infection,
cardiopulmonary
health,
especially
concerning
pulmonary
hypertension
related
disorders.
These
enlightening
discussions
not
only
heightened
awareness
about
impact
various
pathogenic
microorganisms,
including
fungi,
parasites,
viruses,
onset
development
vascular
but
also
cast
spotlight
co‐infections
neglected
illnesses
like
schistosomiasis
‐
disease
that
continues
impose
heavy
socioeconomic
burden
numerous
regions
worldwide.
Thus,
overall
goal
this
review
article
is
present
most
recent
breakthroughs
from
PVDs
as
well
bring
light
scientific
insights
2023
iPVDc/PVRI
symposium
series,
shaping
our
crucial
health
issues
more
than
ever
interconnected
world.
JAMA Pediatrics,
Journal Year:
2022,
Volume and Issue:
176(10), P. 1000 - 1000
Published: Aug. 23, 2022
The
postacute
sequelae
of
SARS-CoV-2
infection
(PASC)
has
emerged
as
a
long-term
complication
in
adults,
but
current
understanding
the
clinical
presentation
PASC
children
is
limited.To
identify
diagnosed
symptoms,
health
conditions,
and
medications
associated
with
children.This
retrospective
cohort
study
used
electronic
records
from
9
US
children's
hospitals
for
individuals
younger
than
21
years
who
underwent
antigen
or
reverse
transcriptase-polymerase
chain
reaction
(RT-PCR)
testing
between
March
1,
2020,
October
31,
2021,
had
at
least
1
encounter
3
before
testing.SARS-CoV-2
positivity
by
viral
test
(antigen
RT-PCR).Syndromic
(symptoms),
systemic
(conditions),
medication
features
were
identified
28
to
179
days
following
initial
date.
Adjusted
hazard
ratios
(aHRs)
obtained
151
clinically
predicted
contrasting
test-positive
groups
test-negative
using
proportional
hazards
models,
adjusting
site,
age,
sex,
location,
race
ethnicity,
time
period
entrance.
incidence
proportion
any
syndromic,
systemic,
feature
was
estimated
2
obtain
burden
estimate.Among
659
286
sample,
348
091
(52.8%)
male,
mean
(SD)
age
8.1
(5.7)
years.
A
total
59
893
(9.1%)
tested
positive
SARS-CoV-2,
599
393
(90.9%)
negative.
Most
outpatient
facility
settings
(322
813
[50.3%])
office
(162
138
[24.6%]).
most
common
loss
taste
smell
(aHR,
1.96;
95%
CI,
1.16-3.32),
myocarditis
3.10;
1.94-4.96),
cough
cold
preparations
1.52;
1.18-1.96),
respectively.
41.9%
(95%
41.4-42.4)
among
vs
38.2%
38.1-38.4)
children,
an
difference
3.7%
3.2-4.2).
higher
strength
association
those
cared
intensive
care
unit
during
acute
illness
phase,
5
years,
complex
chronic
conditions.In
this
large-scale,
exploratory
study,
pediatric
that
presented
systems
low.
Myocarditis
commonly
PASC-associated
condition.
Acute
severity,
young
comorbid
disease
increased
risk
PASC.
The Lancet Regional Health - Europe,
Journal Year:
2022,
Volume and Issue:
18, P. 100394 - 100394
Published: April 29, 2022
The
objective
of
this
study
was
to
describe
12-month
mortality
following
SARS-CoV-2
infection
compared
with
a
reference
population
no
history
SARS-CoV-2.Nationwide
cohort
using
electronic
health
care
data
on
RNA
positive
cases
(n=
66,287)
and
group
subjects
(n=254,969)
linkage
testing
death
records.People
infected
SARS-COV-2
had
more
than
three
times
the
risk
dying
over
year
those
who
remained
uninfected
(aHR
3·1,
95%CI
2·9-3·3).
Short-term
(up
5
weeks
post-infection)
significantly
higher
among
COVID-19
(1623·0/10
000)
in
(118/10
000).
For
aged
60
years
or
older,
increased
persisted
until
end
first
after
infection,
related
for
cardiovascular
2·1,
1·8-2·3),
cancer
1·5,
1·2-1·9),
respiratory
system
diseases
1·9,
1·2-3·0),
other
causes
1·8,
1·4-2·2).Increased
from
is
not
limited
acute
illness:
carries
substantially
12
months.
This
excess
mainly
occurs
older
people
driven
by
broad
array
death.Research
carried
out
support
Estonian
Research
Council
(grants
PRG1197,
PRG198),
European
Regional
Development
Fund
(RITA
1/02-120)
Social
via
IT
Academy
program.
Journal of Clinical Investigation,
Journal Year:
2023,
Volume and Issue:
133(16)
Published: Aug. 14, 2023
The
pulmonary
vasculature
has
been
frequently
overlooked
in
acute
and
chronic
lung
diseases,
such
as
respiratory
distress
syndrome
(ARDS),
fibrosis
(PF),
obstructive
disease
(COPD).
primary
emphasis
the
management
of
these
parenchymal
disorders
largely
revolved
around
injury
aberrant
repair
epithelial
cells.
However,
there
is
increasing
evidence
that
vascular
endothelium
plays
an
active
role
development
diseases.
endothelial
cell
network
capillary
bed
arterial
venous
vessels
provides
a
metabolically
highly
barrier
controls
migration
immune
cells,
regulates
tone
permeability,
participates
remodeling
processes.
Phenotypically
functionally
altered
remodeled
vessels,
can
be
found
although
to
different
degrees,
likely
because
disease-specific
mechanisms.
Since
associated
with
hypertension,
which
worsens
patient
outcomes
survival,
it
crucial
understand
underlying
alterations.
In
this
Review,
we
describe
current
knowledge
regarding
progression
ARDS,
PF,
COPD;
also
outline
future
research
directions
hope
facilitating
mechanism-based
therapies.
Signal Transduction and Targeted Therapy,
Journal Year:
2023,
Volume and Issue:
8(1)
Published: July 14, 2023
Abstract
Exposure
to
the
spike
protein
or
receptor-binding
domain
(S-RBD)
of
SARS-CoV-2
significantly
influences
endothelial
cells
and
induces
pulmonary
vascular
endotheliopathy.
In
this
study,
angiotensin-converting
enzyme
2
humanized
inbred
(hACE2
Tg)
mice
cultured
were
used
investigate
how
protein/S-RBD
impacts
endothelium.
Results
show
that
S-RBD
leads
acute-to-prolonged
induction
intracellular
free
calcium
concentration
([Ca
2+
]
i
)
via
acute
activation
TRPV4,
prolonged
upregulation
mechanosensitive
channel
Piezo1
store-operated
(SOCC)
key
component
Orai1
in
human
arterial
(PAECs).
mechanism,
interacts
with
ACE2
induce
formation
clusters
involving
Orai1,
TRPC1,
facilitate
SOCC,
lead
elevated
apoptosis.
These
effects
are
blocked
by
Kobophenol
A,
which
inhibits
binding
between
ACE2,
chelator,
BAPTA-AM.
Blockade
SOCC
GsMTx4
effectively
protects
S-RBD-induced
microvascular
damage
hACE2
Tg
normalizing
[Ca
.
Comparing
prototypic
strain,
Omicron
variants
(BA.5.2
XBB)
less
severe
cell
Transcriptomic
analysis
indicates
confers
more
than
Delta
Lambda
S-RBD.
summary,
study
provides
compelling
evidence
could
persistent
triggering
through
Orai1.
Targeted
inhibition
ACE2-Piezo1/SOCC-[Ca
axis
proves
a
powerful
strategy
treat
diseases.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(9), P. 4941 - 4941
Published: April 30, 2024
Despite
the
end
of
pandemic,
coronavirus
disease
2019
(COVID-19)
remains
a
major
public
health
concern.
The
first
waves
virus
led
to
better
understanding
its
pathogenesis,
highlighting
fact
that
there
is
specific
pulmonary
vascular
disorder.
Indeed,
COVID-19
may
predispose
patients
thrombotic
in
both
venous
and
arterial
circulation,
many
cases
severe
acute
embolism
have
been
reported.
demonstrated
presence
respiratory
syndrome
2
(SARS-CoV-2)
within
endothelial
cells
suggests
direct
viral
effects,
addition
indirect
effects
perivascular
inflammation
coagulopathy,
contribute
vasculopathy
COVID-19.
In
this
review,
we
discuss
pathological
mechanisms
leading
damage
during
infection,
which
appear
be
mainly
related
thromboembolic
events,
an
impaired
coagulation
cascade,
micro-
macrovascular
thrombosis,
endotheliitis
hypoxic
vasoconstriction.
As
develop
post-COVID
symptoms,
including
dyspnea,
also
hypothesis
hypertension
as
sequela
involved
pathophysiology
long
COVID.