Cardiovascular Innovations and Applications,
Journal Year:
2023,
Volume and Issue:
8(1)
Published: Jan. 1, 2023
Coronavirus
disease
2019
(COVID-19),
caused
by
severe
acute
respiratory
syndrome
coronavirus-2
(SARS-CoV-2),
has
rapidly
become
a
global
health
emergency.
In
addition
to
causing
effects,
SARS-CoV-2
can
result
in
cardiac
involvement
leading
myocardial
damage,
which
is
increasingly
being
explored
the
literature.
Myocardial
injury
an
important
pathogenic
feature
of
COVID-19.
The
angiotensin-converting
enzyme-2
receptor
plays
key
role
pathogenesis
virus,
serving
as
“bridge”
allowing
invade
body.
However,
exact
mechanism
underlying
how
causes
remains
unclear.
This
review
summarizes
main
possible
mechanisms
patients
with
COVID-19,
including
direct
cell
injury,
microvascular
dysfunction,
cytokine
responses
and
systemic
inflammation,
hypoxemia,
stress
responses,
drug-induced
injury.
Understanding
would
aid
proper
identification
treatment
Journal of Biological Chemistry,
Journal Year:
2023,
Volume and Issue:
299(6), P. 104763 - 104763
Published: April 28, 2023
Coronavirus
disease
2019
(COVID-19)
is
a
respiratory
infection
caused
by
severe
acute
syndrome
coronavirus
2.
The
virus
binds
to
angiotensinogen
converting
enzyme
2
(ACE2),
which
mediates
viral
entry
into
mammalian
cells.
COVID-19
notably
in
the
elderly
and
those
with
underlying
chronic
conditions.
cause
of
selective
severity
not
well
understood.
Here
we
show
cholesterol
signaling
lipid
phosphatidyl-inositol
4,5
bisphosphate
(PIP2)
regulate
infectivity
through
localization
ACE2's
nanoscopic
(<200
nm)
clusters.
Uptake
cell
membranes
(a
condition
common
disease)
causes
ACE2
move
from
PIP2
lipids
endocytic
ganglioside
(GM1)
lipids,
where
optimally
located
for
entry.
In
mice,
age
high-fat
diet
increase
lung
tissue
up
40%.
And
smokers
disease,
elevated
2-fold,
magnitude
change
that
dramatically
increases
culture.
We
conclude
increasing
location
near
may
help
explain
aged
diseased
populations.
JACC Advances,
Journal Year:
2024,
Volume and Issue:
3(8), P. 101107 - 101107
Published: July 17, 2024
The
incidence
of
atherosclerotic
cardiovascular
disease
is
increasing
globally,
especially
in
low-
and
middle-income
countries,
despite
significant
efforts
to
reduce
traditional
risk
factors.
Premature
subclinical
atherosclerosis
has
been
documented
association
with
several
viral
infections.
magnitude
the
recent
COVID-19
pandemic
highlighted
need
understand
between
SARS-CoV-2
atherosclerosis.
This
review
examines
various
pathophysiological
mechanisms,
including
endothelial
dysfunction,
platelet
activation,
inflammatory
immune
hyperactivation
triggered
by
infection,
specific
attention
on
their
roles
initiating
promoting
progression
lesions.
Additionally,
it
addresses
pathogenic
mechanisms
which
post-acute
phase
may
contribute
development
vascular
disease.
Understanding
overlap
these
syndromes
enable
novel
therapeutic
strategies.
We
further
explore
for
guidelines
closer
follow-up
often-overlooked
evidence
among
patients
COVID-19,
particularly
those
cardiometabolic
PLoS ONE,
Journal Year:
2025,
Volume and Issue:
20(1), P. e0312402 - e0312402
Published: Jan. 3, 2025
SARS-CoV-2
has
continued
spreading
around
the
world
in
recent
years
since
initial
outbreak
2019,
frequently
developing
into
new
variants
with
greater
human
infectious
capacity.
and
its
mutants
use
angiotensin-converting
enzyme
2
(ACE2)
as
a
cellular
entry
receptor,
which
triggered
several
therapeutic
strategies
against
COVID-19
relying
on
of
ACE2
recombinant
proteins
decoy
receptors.
In
this
work,
we
propose
an
silent
Fc
fusion
protein
(ACE2-hFcLALA)
candidate
therapy
COVID-19.
This
was
able
to
block
binding
RBD
receptor
measured
by
ELISA
flow
cytometry
inhibition
assays.
Moreover,
used
classical
neutralization
assays
progeny
assay
show
that
ACE2-hFcLALA
is
capable
neutralizing
authentic
virus.
Additionally,
found
more
effective
preventing
vitro
infection
different
interest
(
alpha
,
beta
delta
omicron
)
compared
D614G
strain.
Our
results
suggest
potential
molecule
be
both
preventive
settings
current
emerging
gateway
cells.
Vaccines,
Journal Year:
2023,
Volume and Issue:
11(2), P. 204 - 204
Published: Jan. 17, 2023
Since
the
spread
of
deadly
virus
SARS-CoV-2
in
late
2019,
researchers
have
restlessly
sought
to
unravel
how
enters
host
cells.
Some
proteins
on
each
side
interaction
between
and
cells
are
involved
as
major
contributors
this
process:
(1)
nano-machine
spike
protein
behalf
virus,
(2)
angiotensin
converting
enzyme
II,
mono-carboxypeptidase
key
component
renin
system
cell,
(3)
some
proteases
exploited
by
SARS-CoV-2.
In
review,
complex
process
entrance
into
with
contribution
well
sequential
conformational
changes
tending
increase
probability
complexification
latter
receptor
cells,
discussed.
Moreover,
release
catalytic
ectodomain
II
its
soluble
form
extracellular
space
positive
or
negative
impact
infectivity
considered.
Acta Neuropathologica Communications,
Journal Year:
2023,
Volume and Issue:
11(1)
Published: Oct. 2, 2023
Abstract
Cognitive
decline
due
to
Alzheimer’s
disease
(AD)
is
frequent
in
the
geriatric
population,
which
has
been
disproportionately
affected
by
COVID-19
pandemic.
In
this
study,
we
investigated
levels
of
angiotensin-converting
enzyme
2
(ACE2),
a
regulator
renin-angiotensin
system
and
main
entry
receptor
SARS-CoV-2
host
cells,
postmortem
parietal
cortex
samples
from
two
independent
AD
cohorts,
totalling
142
persons.
Higher
concentrations
ACE2
protein
(p
<
0.01)
mRNA
were
found
individuals
with
neuropathological
diagnosis
compared
age-matched
healthy
control
subjects.
Brain
soluble
inversely
associated
cognitive
scores
=
0.02)
markers
pericytes
(PDGFRβ,
p
0.02
ANPEP,
0.007),
but
positively
correlated
amyloid-β
peptides
(Aβ)
insoluble
phospho-tau
(S396/404,
0.002).
However,
no
significant
differences
observed
3xTg-AD
mouse
model
tau
Aβ
neuropathology.
Results
immunofluorescence
Western
blots
showed
that
predominantly
localized
microvessels
brain
whereas
it
more
frequently
neurons
human
brain.
The
present
data
suggest
higher
may
contribute
AD,
their
role
CNS
infection
remains
unclear.
Journal of Infection and Public Health,
Journal Year:
2023,
Volume and Issue:
16(9), P. 1386 - 1391
Published: June 26, 2023
The
COVID-19
pandemic
has
resulted
in
a
global
humanitarian
crisis.
Despite
ongoing
research,
transmission
risks
and
many
disease
characteristics
remain
unclear.
Most
patients
have
displayed
elevated
levels
of
certain
inflammatory
markers,
which
we
sought
to
investigate
further
relation
severity.
aim
this
study
was
examine
the
correlation
between
markers
severity
among
patients.
We
conducted
cross-sectional
from
April
September
2020,
involving
143
PCR-positive
Ziauddin
Hospital.
Electronic
patient
records
provided
data
on
demographics,
clinical
status,
laboratory
results.
majority
were
elderly
males
with
comorbidities
such
as
diabetes
hypertension.
Almost
all
exhibited
increased
various
procalcitonin
(97.2%)
being
most
common.
Statistically
significant
differences
observed
TLC
(p=0.005),
CRP
(p=0.001),
LDH
Ferritin
D-dimer
(p=0.028),
suggest
association
All
except
procalcitonin,
demonstrated
These
results
could
enhance
our
understanding
pathogenesis
help
predict
manage
severe
cases.
Scientific Reports,
Journal Year:
2023,
Volume and Issue:
13(1)
Published: Feb. 27, 2023
A
highly
contagious
virus,
severe
acute
respiratory
syndrome
coronavirus
2,
caused
the
disease
19
(COVID-19)
pandemic
(SARS-CoV-2).
SARS-CoV-2
genetic
variants
have
been
reported
to
circulate
throughout
COVID-19
pandemic.
symptoms
include
symptoms,
fever,
muscle
pain,
and
breathing
difficulty.
In
addition,
up
30%
of
patients
experience
neurological
complications
such
as
headaches,
nausea,
stroke,
anosmia.
However,
neurotropism
infection
remains
largely
unknown.
This
study
investigated
neurotropic
patterns
between
B1.617.2
(Delta)
Hu-1
(Wuhan,
early
strain)
in
K18-hACE2
mice.
Despite
both
inducing
similar
pathogenic
various
organs,
B1.617.2-infected
mice
demonstrated
a
higher
range
phenotypes
weight
loss,
lethality,
conjunctivitis
when
compared
those
Hu-1-infected
histopathological
analysis
revealed
that
infects
brain
more
rapidly
effectively
than
Hu-1.
Finally,
we
discovered
that,
mice,
activation
signature
genes
involved
innate
cytokines
necrosis-related
response
was
most
pronounced
The
present
findings
indicate
neuroinvasive
properties
link
them
fatal
neuro-dissemination
during
onset.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(6), P. 5374 - 5374
Published: March 11, 2023
The
clinical
manifestations
of
the
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
infection
responsible
for
disease
2019
(COVID-19)
commonly
include
dyspnoea
and
fatigue,
they
primarily
involve
lungs.
However,
extra-pulmonary
organ
dysfunctions,
particularly
affecting
cardiovascular
system,
have
also
been
observed
following
COVID-19
infection.
In
this
context,
several
cardiac
complications
reported,
including
hypertension,
thromboembolism,
arrythmia
heart
failure,
with
myocardial
injury
myocarditis
being
most
frequent.
These
secondary
inflammatory
responses
appear
to
be
associated
a
poorer
course
increased
mortality
in
patients
COVID-19.
addition,
numerous
episodes
reported
as
complication
mRNA
vaccinations,
especially
young
adult
males.
Changes
cell
surface
expression
angiotensin-converting
enzyme
(ACE2)
direct
cardiomyocytes
resulting
from
exaggerated
immune
are
just
some
mechanisms
that
may
explain
pathogenesis
COVID-19-induced
myocarditis.
Here,
we
review
pathophysiological
underlying
infection,
particular
focus
on
involvement
ACE2
Toll-like
receptors
(TLRs).