Cellular & Molecular Biology Letters,
Год журнала:
2024,
Номер
29(1)
Опубликована: Ноя. 8, 2024
Coronavirus
disease
2019
(COVID-19)
represents
the
novel
respiratory
infectious
disorder
caused
by
severe
acute
syndrome
coronavirus
2
(SARS-CoV-2)
and
is
characterized
rapid
spread
throughout
world.
Reactive
oxygen
species
(ROS)
account
for
cellular
metabolic
by-products,
excessive
ROS
accumulation
can
induce
oxidative
stress
due
to
insufficient
endogenous
antioxidant
ability.
In
case
of
stress,
production
exceeds
capacity,
thus
leading
cell
death.
SARS-CoV-2
activate
different
death
pathways
in
context
infection
host
cells,
such
as
neutrophil
extracellular
trap
(NET)osis,
ferroptosis,
apoptosis,
pyroptosis,
necroptosis
autophagy,
which
are
closely
related
signalling
control.
this
review,
we
comprehensively
elucidated
relationship
between
generation
cells
after
infection,
leads
development
COVID-19,
aiming
provide
a
reasonable
basis
existing
interventions
further
therapies
against
SARS-CoV-2.
Sepsis
is
a
life-threatening
condition
resulting
from
pathogen
infection
and
characterized
by
organ
dysfunction.
Programmed
cell
death
(PCD)
during
sepsis
has
been
associated
with
the
development
of
multiple
dysfunction
syndrome
(MODS),
impacting
various
physiological
systems
including
respiratory,
cardiovascular,
renal,
neurological,
hematological,
hepatic,
intestinal
systems.
It
well-established
that
infections
lead
to
immune
dysregulation,
which
subsequently
contributes
MODS
in
sepsis.
However,
recent
evidence
suggests
sepsis-related
opportunistic
pathogens
can
directly
induce
failure
promoting
PCD
parenchymal
cells
each
affected
organ.
This
study
provides
an
overview
damaged
induction
host
pathogens,
proposing
innovative
strategies
for
preventing
Cell Death and Disease,
Год журнала:
2023,
Номер
14(4)
Опубликована: Апрель 29, 2023
Abstract
Coronavirus
disease
(COVID-19)
is
a
contagious
respiratory
caused
by
the
SARS-CoV-2
virus.
The
clinical
phenotypes
are
variable,
ranging
from
spontaneous
recovery
to
serious
illness
and
death.
On
March
2020,
global
COVID-19
pandemic
was
declared
World
Health
Organization
(WHO).
As
of
February
2023,
almost
670
million
cases
6,8
deaths
have
been
confirmed
worldwide.
Coronaviruses,
including
SARS-CoV-2,
contain
single-stranded
RNA
genome
enclosed
in
viral
capsid
consisting
four
structural
proteins:
nucleocapsid
(N)
protein,
ribonucleoprotein
core,
spike
(S)
envelope
(E)
membrane
(M)
embedded
surface
envelope.
In
particular,
E
protein
poorly
characterized
viroporin
with
high
identity
amongst
all
β-coronaviruses
(SARS-CoV-2,
SARS-CoV,
MERS-CoV,
HCoV-OC43)
low
mutation
rate.
Here,
we
focused
our
attention
on
study
M
proteins,
found
general
perturbation
host
cell
calcium
(Ca
2+
)
homeostasis
selective
rearrangement
interorganelle
contact
sites.
vitro
vivo
biochemical
analyses
revealed
that
binding
specific
nanobodies
soluble
regions
reversed
observed
phenotypes,
suggesting
might
be
an
important
therapeutic
candidate
not
only
for
vaccine
development,
but
also
management
COVID
designing
drug
regimens
that,
so
far,
very
limited.
Frontiers in Immunology,
Год журнала:
2023,
Номер
14
Опубликована: Дек. 22, 2023
Significance
This
review
discusses
the
coronavirus
disease
2019
(COVID-19)
pathophysiology
in
context
of
diabetes
and
intracellular
reactions
by
COVID-19,
including
mitochondrial
oxidative
stress
storms,
ROS
long
COVID.
Recent
advances
The
COVID
is
suffered
~10%
COVID-19
patients.
Even
virus
does
not
exist,
patients
suffer
for
even
over
a
year,
could
be
mitochondria
dysregulation
disease.
Critical
issues
Patients
who
recover
from
can
develop
new
or
persistent
symptoms
multi-organ
complications
lasting
weeks
months,
called
underlying
mechanisms
involved
still
unclear.
Once
persist,
they
cause
significant
damage,
leading
to
numerous,
symptoms.
Future
directions
A
comprehensive
map
stages
pathogenetic
related
effective
drugs
treat
prevent
it
are
required,
which
will
aid
development
future
treatments
symptom
relief.
Folia Biologica,
Год журнала:
2024,
Номер
70(1), С. 45 - 52
Опубликована: Янв. 1, 2024
Effective
treatment
of
patients
with
autism
spectrum
disorder
(ASD)
is
still
absent
so
far.
Taurine
exhibits
therapeutic
effects
towards
the
autism-like
behaviour
in
ASD
model
animals.
Here,
we
determined
mechanism
taurine
effect
on
hippocampal
neurogenesis
genetically
inbred
BTBR
T
+
tf/J
(BTBR)
mice,
a
proposed
ASD.
In
this
mouse
model,
explored
oral
supplementation
ASD-like
behaviours
an
open
field
test,
elevated
plus
maze,
marble
burying
self-grooming
and
three-chamber
test.
The
mice
were
divided
into
four
groups
normal
controls
(WT)
models
(BTBR),
who
did
or
not
receive
6-week
water
(WT,
WT+
Taurine,
BTBR,
BTBR+Taurine).
Neurogenesis-related
by
Ki67
immunofluorescence
staining.
Western
blot
analysis
was
performed
to
detect
expression
phosphatase
tensin
homologue
deleted
from
chromosome
10
(PTEN)/mTOR/AKT
pathway-associated
proteins.
Our
results
showed
that
improved
behaviour,
increased
proliferation
cells,
promoted
PTEN
expression,
reduced
phosphorylation
mTOR
AKT
tissue
mice.
conclusion,
partially
inherited
which
may
be
associated
improving
defective
neural
precursor
cell
enhancing
PTEN-associated
pathway
tissue.
Cell Death and Differentiation,
Год журнала:
2022,
Номер
30(3), С. 731 - 741
Опубликована: Окт. 26, 2022
Abstract
BOK
is
a
poorly
understood
member
of
the
BCL-2
family
proteins
that
has
been
proposed
to
function
as
pro-apoptotic,
BAX-like
effector.
However,
molecular
mechanism
and
structural
properties
pores
remain
enigmatic.
Here,
we
show
thermal
stability
pore
activity
depends
on
presence
its
C-terminus
well
mitochondrial
lipid
cardiolipin.
We
directly
visualized
in
liposomes
by
electron
microscopy,
which
appeared
similar
those
induced
BAX,
line
with
comparable
oligomerization
quantified
single
molecule
imaging.
In
addition,
super-resolution
STED
imaging
revealed
organized
into
dots
ring-shaped
assemblies
apoptotic
mitochondria,
also
reminiscent
found
for
BAX
BAK.
Yet,
unlike
BAK,
was
limited
partial
localization
independent
unaffected
other
proteins.
These
results
suggest
that,
while
kept
check
subcellular
instead
interaction
members,
resulting
are
structurally
Abstract
There
is
still
a
significant
lack
of
knowledge
regarding
many
aspects
the
etiopathology
and
consequences
severe
acute
respiratory
syndrome
coronavirus
2
(SARS‐CoV‐2)
infection
in
humans.
For
example,
variety
molecular
mechanisms
mediating
this
infection,
long‐term
disease
remain
poorly
understood.
It
first
seemed
like
SARS‐CoV‐2
primarily
caused
serious
syndrome.
However,
over
last
years,
an
increasing
number
studies
also
pointed
towards
damaging
effects
has
on
central
nervous
system
(CNS).
In
fact,
evidence
suggests
possible
disruption
blood–brain
barrier
deleterious
CNS,
especially
patients
who
already
suffer
from
other
pathologies,
such
as
neurodegenerative
disorders.
The
behind
these
CNS
could
involve
dysregulation
mitochondrial
physiology,
well‐known
early
marker
neurodegeneration
hallmark
aging.
Moreover,
mitochondria
are
involved
activation
inflammatory
response,
which
been
broadly
described
COVID‐19.
Here,
we
critically
review
current
bibliography
presence
symptoms
COVID‐19
patients,
with
special
emphasis
Microorganisms,
Год журнала:
2024,
Номер
12(2), С. 332 - 332
Опубликована: Фев. 4, 2024
Coronavirus
disease
2019
(COVID-19)
caused
a
severe
epidemic
due
to
acute
respiratory
syndrome
coronavirus-2
(SARS-CoV-2).
Recent
studies
have
found
that
patients
do
not
completely
recover
from
infections,
but
instead,
suffer
variety
of
post-acute
sequelae
SARS-CoV-2
infection,
known
as
long
COVID.
The
effects
COVID
can
be
far-reaching,
with
duration
up
six
months
and
range
symptoms
such
cognitive
dysfunction,
immune
dysregulation,
microbiota
dysbiosis,
myalgic
encephalomyelitis/chronic
fatigue
syndrome,
myocarditis,
pulmonary
fibrosis,
cough,
diabetes,
pain,
reproductive
thrombus
formation.
However,
recent
shown
naringenin
naringin
palliative
on
various
COVID-19
sequelae.
Flavonoids
naringenin,
commonly
in
fruits
vegetables,
positive
effects,
including
reducing
inflammation,
preventing
viral
providing
antioxidants.
This
article
discusses
the
molecular
mechanisms
clinical
treating
above
diseases.
It
proposes
them
potential
drugs
for
treatment
COVID,
it
inferred
exhibit
extended
medications,
future
likely
serving
nutraceuticals
or
supplements
comprehensive
alleviation
manifestations
complications.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(6), С. 3096 - 3096
Опубликована: Март 7, 2024
Porcine
epidemic
diarrhea
virus
(PEDV),
a
member
of
the
Alpha-coronavirus
genus
in
Coronaviridae
family,
induces
acute
diarrhea,
vomiting,
and
dehydration
neonatal
piglets.
This
study
aimed
to
investigate
genetic
dependencies
PEDV
identify
potential
therapeutic
targets
by
using
single-guide
RNA
(sgRNA)
lentiviral
library
screen
host
factors
required
for
infection.
Protein
kinase
C
θ
(PKCθ),
calcium-independent
PKC
family
localized
cell
membrane,
was
found
be
crucial
factor
The
investigation
infection
limited
Vero
porcine
epithelial
cell-jejunum
2
(IPEC-J2)
due
defective
interferon
production
poor
replication
IPEC-J2.
Therefore,
identifying
suitable
cells
is
crucial.
findings
this
reveal
that
human
embryonic
kidney
(HEK)
293T
L929
cells,
but
not
IPEC-J2
were
investigating
PKCθ
played
significant
role
endocytosis
PEDV,
regulated
expression
phosphorylation
PKCθ.
Apoptosis
involved
replication,
as
activated
PKCθ-B-cell
lymphoma
(BCL-2)
ovarian
killer
(BOK)
axis
HEK293T
increase
viral
via
mitochondrial
apoptosis.
demonstrated
suitability
identified
essential
These
provide
valuable
insights
development
strategies
drug