Frontiers in Immunology,
Год журнала:
2022,
Номер
13
Опубликована: Март 2, 2022
Infection
with
SARS-CoV-2,
the
causative
agent
of
Coronavirus
disease
2019
(COVID-19)
pandemic,
causes
respiratory
problems
and
multifaceted
organ
dysfunction.
A
crucial
mechanism
COVID-19
immunopathy
is
recruitment
activation
neutrophils
at
infection
site,
which
also
predicts
severity
poor
outcomes.
The
release
neutrophil
extracellular
traps
(NETs),
occurring
during
a
regulated
form
cell
death
known
as
NETosis,
key
effector
function
that
mediates
harmful
effects
caused
by
neutrophils.
Abundant
NETosis
NET
generation
have
been
observed
in
many
patients,
leading
to
unfavorable
coagulopathy
immunothrombosis.
Moreover,
excessive
are
now
more
widely
recognized
mediators
additional
pathophysiological
abnormalities
following
SARS-CoV-2
infection.
In
this
minireview,
we
introduce
subtypes
NET-producing
(e.g.,
low-density
granulocytes)
explain
biological
importance
NETs
protein
cargos
COVID-19.
addition,
discuss
mechanisms
upregulating
viral
processes
entry
replication)
well
host
pro-NET
proinflammatory
mediator
release,
platelet
activation,
autoantibody
production).
Furthermore,
provide
an
update
main
findings
immunothrombosis
other
COVID-19-related
disorders,
such
aberrant
immunity,
neurological
post
syndromes
including
lung
fibrosis,
disorder,
tumor
progression,
deteriorated
chronic
illness.
Finally,
address
potential
prospective
treatment
strategies
target
dysregulated
formation
via
inhibition
promotion
degradation,
respectively.
Chinese Medical Journal - Pulmonary and Critical Care Medicine,
Год журнала:
2023,
Номер
1(2), С. 77 - 83
Опубликована: Янв. 23, 2023
The
pandemic
of
coronavirus
disease
2019
(COVID‑19),
caused
by
a
novel
severe
acute
respiratory
syndrome
(SARS)
2
(SARS-CoV-2),
has
an
enormous
impact
on
the
global
healthcare.
SARS-CoV-2
infection
primarily
targets
system.
Although
most
individuals
testing
positive
for
present
mild
or
no
upper
tract
symptoms,
patients
with
COVID-19
can
rapidly
progress
to
distress
(ARDS).
ARDS-related
pulmonary
fibrosis
is
recognized
sequelae
COVID-19.
Whether
post-COVID-19
lung
resolvable,
persistent,
even
becomes
progressive
as
seen
in
human
idiopathic
(IPF)
currently
not
known
and
remains
matter
debate.
With
emergence
effective
vaccines
treatments
against
COVID-19,
it
now
important
build
our
understanding
long-term
sequela
infection,
identify
survivors
who
are
at
risk
developing
chronic
fibrosis,
develop
anti-fibrotic
therapies.
current
review
aims
summarize
pathogenesis
system
highlights
potential
mechanisms.
It
envisions
fibrotic
complication
survivors,
particular
aged
population.
early
identification
development
therapies
discussed.
Lipids in Health and Disease,
Год журнала:
2024,
Номер
23(1)
Опубликована: Апрель 3, 2024
Abstract
Pulmonary
fibrosis
(PF)
is
a
severe
pulmonary
disease
with
limited
available
therapeutic
choices.
Recent
evidence
increasingly
points
to
abnormal
lipid
metabolism
as
critical
factor
in
PF
pathogenesis.
Our
latest
research
identifies
the
dysregulation
of
low-density
lipoprotein
(LDL)
new
risk
for
PF,
contributing
alveolar
epithelial
and
endothelial
cell
damage,
fibroblast
activation.
In
this
study,
we
first
integrative
summarize
published
literature
about
metabolite
changes
found
including
phospholipids,
glycolipids,
steroids,
fatty
acids,
triglycerides,
lipoproteins.
We
then
reanalyze
two
single-cell
RNA-sequencing
(scRNA-seq)
datasets
corresponding
metabolomic
genes
responsible
these
lipids’
biosynthesis,
catabolism,
transport,
modification
processes
are
uncovered.
Intriguingly,
that
macrophage
most
active
type
metabolism,
almost
all
metabolic
being
altered
macrophages
PF.
2
cells,
differentially
expressed
(DEGs)
primarily
associated
cytidine
diphosphate
diacylglycerol
pathway,
cholesterol
triglyceride
synthesis.
Endothelial
cells
partly
sphingomyelin,
phosphatidylcholine,
phosphatidylethanolamines
reprogramming
their
dysregulated
Fibroblasts
may
contribute
cholesterol,
phosphatidylethanolamine
Therefore,
reprogrammed
profiles
be
attributed
aberrant
expression
different
types.
Taken
together,
insights
underscore
potential
targeting
developing
innovative
strategies,
potentially
leading
extended
overall
survival
individuals
affected
by
Cell Death and Disease,
Год журнала:
2022,
Номер
13(12)
Опубликована: Дек. 24, 2022
Abstract
Pulmonary
fibrosis
(PF),
as
an
end-stage
clinical
phenotype
of
interstitial
lung
diseases
(ILDs),
is
frequently
initiated
after
alveolar
injury,
in
which
ferroptosis
has
been
identified
a
critical
event
aggravating
the
pathophysiological
progression
this
disease.
Here
in,
comprehensive
analysis
two
mouse
models
pulmonary
developed
our
lab
demonstrated
that
damage-induced
epithelial
Type2
cells
(AEC2)
significantly
accumulates
during
development
while
suppressor
genes
GPX4
and
FSP1
are
dramatically
inactivated.
Mechanistically,
upregulation
de
novo
methylation
regulator
Uhrf1
sensitively
elevates
CpG
site
levels
promoters
both
induces
epigenetic
repression
genes,
subsequently
leading
to
chemically
interfered
AEC2
cells.
Meanwhile,
specific
inhibition
UHRF1
highly
arrests
formation
blocks
research
models.
This
study
first,
knowledge,
involvement
mediating
injured
AEC2s
via
promoter-specific
consequently
accelerates
process
fibrosis.
The
above
findings
also
strongly
suggested
novel
potential
target
treatment
Frontiers in Pharmacology,
Год журнала:
2022,
Номер
13
Опубликована: Март 4, 2022
The
pathogenetic
mechanism
of
post-Covid-19
pulmonary
fibrosis
is
currently
a
topic
intense
research
interest,
but
still
largely
unexplored.
aim
this
work
was
to
carry
out
systematic
exploratory
search
the
literature
(Scoping
review)
identify
and
systematize
main
mechanisms
that
are
believed
be
involved
in
phenomenon,
order
highlight
same
molecular
aspect
lung.
These
aims
could
essential
future
for
therapeutic
management.
We
identified
all
primary
studies
involving
post
COVID19
syndrome
with
as
endpoint
by
performing
data
searches
various
review
databases.
Two
reviewers
independently
reviewed
abstracts
(398)
full
text
data.
quality
study
has
been
assess
through
SANRA
protocol.
A
total
32
were
included,
included
possible
involvement
inflammatory
cytokines,
concerned
renin-angiotensin
system,
potential
role
galectin-3,
epithelial
injuries
fibrosis,
alveolar
type
2
involvement,
Neutrophil
extracellular
traps
(NETs)
others
implied
other
specific
aspects
(relationship
clinical
mechanical
factors,
transition
mesenchymal,
TGF-β
signaling
pathway,
midkine,
caspase
macrophages,
genetics).
In
most
cases,
these
narrative
reviews
or
letters
editor,
except
10
articles,
which
presented
original
data,
albeit
sometimes
experimental
models.
From
development
researches,
progress
knowledge
phenomenon
hopefully
its
prevention
therapy
may
originate.
Infectious Disease Reports,
Год журнала:
2023,
Номер
15(6), С. 806 - 830
Опубликована: Дек. 15, 2023
The
coronavirus
disease
2019
(COVID-19),
instigated
by
the
zoonotic
Severe
Acute
Respiratory
Syndrome
Coronavirus
2
(SARS-CoV-2),
rapidly
transformed
from
an
outbreak
in
Wuhan,
China,
into
a
widespread
global
pandemic.
A
significant
post-infection
condition,
known
as
'long-
COVID-19'
(or
simply
COVID'),
emerges
substantial
subset
of
patients,
manifesting
with
constellation
over
200
reported
symptoms
that
span
multiple
organ
systems.
This
also
'post-acute
sequelae
SARS-CoV-2
infection'
(PASC),
presents
perplexing
clinical
picture
far-reaching
implications,
often
persisting
long
after
acute
phase.
While
initial
research
focused
on
immediate
pulmonary
impact
virus,
recognition
COVID-19
multiorgan
disruptor
has
unveiled
gamut
protracted
and
severe
health
issues.
review
summarizes
primary
effects
COVID
respiratory,
cardiovascular,
nervous
It
delves
mechanisms
underlying
these
impacts
underscores
critical
need
for
comprehensive
understanding
COVID's
pathogenesis.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(3), С. 1562 - 1562
Опубликована: Янв. 26, 2024
The
COVID-19
pandemic
has
had
a
significant
impact
on
the
health
and
economy
of
global
population.
Even
after
recovery
from
disease,
post-COVID-19
symptoms,
such
as
pulmonary
fibrosis,
continue
to
be
concern.
This
narrative
review
aims
address
fibrosis
(PF)
various
perspectives,
including
fibrotic
mechanisms
involved
in
idiopathic
COVID-19-induced
fibrosis.
On
other
hand,
we
also
discuss
current
therapeutic
drugs
use,
well
those
undergoing
clinical
or
preclinical
evaluation.
Additionally,
this
article
will
biomarkers
with
usefulness
for
PF
prediction,
diagnosis,
treatment,
prognosis,
severity
assessment
order
provide
better
treatment
strategies
patients
disease.
