Biomedicines,
Год журнала:
2021,
Номер
9(9), С. 1220 - 1220
Опубликована: Сен. 14, 2021
Background.
Emerging
evidences
suggest
that
in
severe
COVID-19,
multi-organ
failure
is
associated
with
a
hyperinflammatory
state
(the
so-called
“cytokine
storm”)
combination
the
development
of
prothrombotic
state.
The
central
role
endothelial
dysfunction
pathogenesis
disease
to
date
accepted,
but
precise
mechanisms
underlying
coagulopathy
remain
unclear.
Whether
alterations
vascular
homeostasis
directly
depend
upon
SARS-CoV-2
infection
cells
or,
rather,
occur
secondarily
activation
inflammatory
response
still
matter
debate.
Here,
we
address
effect
spike
S1
protein
on
human
lung
microvascular
(HLMVEC).
In
particular,
existence
an
endothelium-macrophage
crosstalk
has
been
explored.
Methods
and
Results.
addressed
(HLMVEC),
either
or
after
incubation
conditioned
medium
(CM)
monocyte-derived
macrophages
(MDM)
previously
activated
by
(CM-MDM).
Both
MDM
HLMVEC
are
protein,
increased
expression
pro-inflammatory
mediators.
However,
when
exposed
CM-MDM,
enhanced
cell
occurs
terms
adhesion
molecules,
pro-coagulant
markers,
chemokines.
Under
this
experimental
condition,
ICAM-1
VCAM-1,
chemokines
CXCL8/IL-8,
CCL2/MCP1,
CXCL10/IP-10
as
well
tissue
factor
(TF)
markedly
induced.
Instead,
decrease
thrombomodulin
(THBD)
observed.
Conclusion.
Our
data
mediators
released
spike-activated
amplify
cells,
likely
contributing
impairment
integrity
pro-coagulative
endothelium.
Cardiovascular Research,
Год журнала:
2022,
Номер
118(15), С. 3085 - 3096
Опубликована: Июнь 16, 2022
Thrombotic
complications
and
vasculopathy
have
been
extensively
associated
with
severe
COVID-19
infection;
however,
the
mechanisms
inducing
endotheliitis
disruption
of
endothelial
integrity
in
microcirculation
are
poorly
understood.
We
hypothesized
that
within
vessel
wall,
pericytes
preferentially
take
up
viral
particles
mediate
subsequent
loss
vascular
integrity.
World Journal of Clinical Cases,
Год журнала:
2023,
Номер
11(1), С. 73 - 83
Опубликована: Янв. 3, 2023
An
outbreak
of
coronavirus
disease
2019
(COVID-19)
has
spread
globally,
with
over
500
million
cases
and
6
deaths
to
date.
COVID-19
is
associated
a
systemic
inflammatory
response
abnormalities
the
extracellular
matrix
(ECM),
which
also
involved
in
storms.
Upon
viral
infection,
ECM
proteins
are
recruitment
cells
interference
target
organ
metabolism,
including
lungs.
Additionally,
serum
biomarkers
turnover
severity
may
serve
as
potential
targets.
Consequently,
understanding
expression
function
ECM,
particularly
lung,
during
severe
acute
respiratory
syndrome
2
infection
would
provide
valuable
insights
into
mechanisms
progression.
In
this
review,
we
summarize
current
findings
on
such
hyaluronic
acid,
metalloproteinases,
collagen,
linked
inflammation
COVID-19.
Some
drugs
targeting
surface
have
been
effective.
future,
these
could
novel
perspectives
pathogenesis
treatment
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(3), С. 1837 - 1837
Опубликована: Фев. 2, 2024
Arterial
hypertension
is
one
of
the
most
common
and
significant
cardiovascular
risk
factors.
There
are
many
well-known
identified
factors
for
its
development.
In
recent
times,
there
has
been
growing
concern
about
potential
impact
COVID-19
on
system
relation
to
arterial
hypertension.
Various
theories
have
developed
that
suggest
a
connection
between
elevated
blood
pressure.
However,
precise
link
SARS-CoV-2
infection
long-term
developing
remains
insufficiently
explored.
Therefore,
primary
objective
our
study
was
investigate
influence
pressure
elevation
subsequent
over
an
extended
period.
To
accomplish
this,
we
conducted
thorough
search
review
relevant
papers
in
PubMed
SCOPUS
databases
up
3
September
2023.
Our
analysis
encompassed
total
30
eligible
articles.
Out
reviewed,
19
them
provided
substantial
evidence
showing
heightened
following
infection.
Eight
studies
showed
values
increased
after
infection,
while
three
qualified
did
not
report
any
notable
levels.
The
mechanism
behind
development
unclear,
but
it
suggested
endothelial
injury
dysfunction
renin-angiotensin-aldosterone
may
be
contributory.
Additionally,
changes
could
linked
lifestyle
alterations
often
occur
alongside
illness.
findings
emphasize
pressing
requirement
research
into
relationship
These
insights
essential
effective
prevention
management
approaches
individuals
who
experienced
Journal of Pharmacology and Experimental Therapeutics,
Год журнала:
2024,
Номер
389(1), С. 34 - 39
Опубликована: Фев. 9, 2024
Emerging
evidence
indicates
that
the
relationship
between
coronavirus
disease
2019
(COVID-19)
and
diabetes
is
2-fold:
1)
it
known
presence
of
other
metabolic
alterations
poses
a
considerably
high
risk
to
develop
severe
COVID-19;
2)
patients
who
survived
acute
respiratory
syndrome
2
(SARS-CoV-2)
infection
have
an
increased
developing
new-onset
diabetes.
However,
mechanisms
underlying
this
association
are
mostly
unknown,
there
no
reliable
biomarkers
predict
development
In
present
study,
we
demonstrate
specific
microRNA
(miR-34a)
contained
in
circulating
extracellular
vesicles
released
by
endothelial
cells
reliably
predicts
COVID-19.
This
was
independent
age,
sex,
body
mass
index
(BMI),
hypertension,
dyslipidemia,
smoking
status,
D-dimer.
SIGNIFICANCE
STATEMENT:
We
for
first
time
able
after
having
contracted
(COVID-19).
Our
findings
also
relevant
when
considering
emerging
importance
post-acute
sequelae
COVID-19,
with
systemic
manifestations
observed
even
months
viral
negativization
(long
COVID).
Biomedicines,
Год журнала:
2021,
Номер
9(9), С. 1220 - 1220
Опубликована: Сен. 14, 2021
Background.
Emerging
evidences
suggest
that
in
severe
COVID-19,
multi-organ
failure
is
associated
with
a
hyperinflammatory
state
(the
so-called
“cytokine
storm”)
combination
the
development
of
prothrombotic
state.
The
central
role
endothelial
dysfunction
pathogenesis
disease
to
date
accepted,
but
precise
mechanisms
underlying
coagulopathy
remain
unclear.
Whether
alterations
vascular
homeostasis
directly
depend
upon
SARS-CoV-2
infection
cells
or,
rather,
occur
secondarily
activation
inflammatory
response
still
matter
debate.
Here,
we
address
effect
spike
S1
protein
on
human
lung
microvascular
(HLMVEC).
In
particular,
existence
an
endothelium-macrophage
crosstalk
has
been
explored.
Methods
and
Results.
addressed
(HLMVEC),
either
or
after
incubation
conditioned
medium
(CM)
monocyte-derived
macrophages
(MDM)
previously
activated
by
(CM-MDM).
Both
MDM
HLMVEC
are
protein,
increased
expression
pro-inflammatory
mediators.
However,
when
exposed
CM-MDM,
enhanced
cell
occurs
terms
adhesion
molecules,
pro-coagulant
markers,
chemokines.
Under
this
experimental
condition,
ICAM-1
VCAM-1,
chemokines
CXCL8/IL-8,
CCL2/MCP1,
CXCL10/IP-10
as
well
tissue
factor
(TF)
markedly
induced.
Instead,
decrease
thrombomodulin
(THBD)
observed.
Conclusion.
Our
data
mediators
released
spike-activated
amplify
cells,
likely
contributing
impairment
integrity
pro-coagulative
endothelium.
