Viruses,
Год журнала:
2024,
Номер
16(11), С. 1694 - 1694
Опубликована: Окт. 30, 2024
SARS-CoV-2
is
highly
transmissible
and
affects
the
respiratory
system.
People
with
COVID-19
are
at
higher
risk
of
physical
mental
health
conditions,
which
could
impact
bone
health.
The
aim
this
review
was
to
explore
effects
on
BMD,
BTMs,
joints.
An
electronic
search
PubMed,
Web
Science,
Scopus,
Ovid
Medline
databases
considered
studies
published
between
1
January
2020
November
2023.
limited
English,
original
in
adult
humans.
title
abstract
identified
papers
were
screened,
followed
by
a
full-text
using
inclusion
exclusion
criteria.
data
extracted
included
study
participant
characteristics,
joint
abnormalities.
Newcastle-Ottawa
scale
quality
assessment
tool
used
assess
bias.
Five
involving
305
out
495
infected
individuals
observed
reduced
BMD
after
COVID-19,
most
significant
reduction
occurring
year
later.
Both
resorption
formation
markers
decreased,
while
regulatory
showed
levels
patients.
may
harm
increasing
reducing
absorption,
leading
lower
BMD.
Elderly,
frail,
osteopenic
or
osteoporotic
should
be
regularly
monitored
for
loss
if
they
have
long
COVID.
Current Osteoporosis Reports,
Год журнала:
2024,
Номер
22(1), С. 122 - 134
Опубликована: Янв. 15, 2024
Abstract
Purpose
of
Review
SARS-CoV-2
drove
the
catastrophic
global
phenomenon
COVID-19
pandemic
resulting
in
a
multitude
systemic
health
issues,
including
bone
loss.
The
purpose
this
review
is
to
summarize
recent
findings
related
loss
and
potential
mechanisms.
Recent
Findings
early
clinical
evidence
indicates
an
increase
vertebral
fractures,
hypocalcemia,
vitamin
D
deficiencies,
BMD
among
patients.
Additionally,
lower
associated
with
more
severe
infection.
Preclinical
models
have
shown
increased
osteoclastogenesis.
infection
could
be
result
many
factors
that
directly
affect
such
as
higher
inflammation,
activation
NLRP3
inflammasome,
recruitment
Th17
cells,
hypoxic
environment,
changes
RANKL/OPG
signaling.
can
exert
indirect
effects
on
skeleton,
mechanical
unloading
may
occur
disease
(e.g.,
bed
rest)
or
BMI
muscle
wasting
has
also
been
Muscle
cause
issues
influence
bone.
Medications
used
treat
negative
effect
Lastly,
worsen
conditions
diabetes
negatively
kidney
function,
all
which
contribute
fracture
risk.
Summary
through
multiple
direct
Future
work
will
needed
determine
what
patient
populations
are
at
risk
COVID-19-related
increases
risk,
mechanisms
behind
loss,
therapeutic
options.
This
article
part
series
manuscripts
designed
utility
using
artificial
intelligence
for
writing
scientific
reviews.
Current Osteoporosis Reports,
Год журнала:
2024,
Номер
22(1), С. 135 - 145
Опубликована: Янв. 18, 2024
SARS-CoV-2
infection,
the
culprit
of
COVID-19
pandemic,
has
been
associated
with
significant
long-term
effects
on
various
organ
systems,
including
bone
health.
This
review
explores
current
understanding
impacts
infection
health
and
its
potential
consequences.
Journal of Cellular and Molecular Medicine,
Год журнала:
2025,
Номер
29(3)
Опубликована: Янв. 31, 2025
Abstract
Molecules
of
the
tumour
necrosis
factor
superfamily
(TNFSF)
are
key
players
in
immune
regulation;
an
increase
some
TNFSF
molecules
has
been
reported
during
severe
COVID‐19.
In
this
study,
we
profiled
and
evaluated
members
serum
COVID‐19
vaccine‐naïve
patients
to
identify
potential
biomarkers
associated
with
disease
severity.
Our
data
show
that
TRAIL
levels
lower
severely
affected
than
those
mildly
by
(AUC
0.8,
p
=
0.0003).
On
contrary,
OPG
BAFF
higher
compared
mild
cases
0.0001;
AUC
0.7,
0.0012;
respectively)
moderate
(OPG
<
0.01),
(
0.05).
At
transcriptional
level,
TRAIL,
elevated
cases,
also
patients.
Additionally,
found
APRIL,
LIGHT,
CD30L
CD40L
protein‐levels
healthy
donors
but
not
significantly
different
between
various
clinical
statuses.
Finally,
TNF‐α,
TNF‐β,
RANKL
TWEAK
protein
were
work
identifies
as
therapeutic
targets
for
preventing
Due
opposite
contradictory
(protein/transcriptional
level),
its
role
should
be
elucidated
clarified
more
in‐depth
studies.
Animal Models and Experimental Medicine,
Год журнала:
2025,
Номер
unknown
Опубликована: Март 3, 2025
Abstract
The
World
Health
Organization
has
declared
that
COVID‐19
no
longer
constitutes
a
“public
health
emergency
of
international
concern,”
yet
the
long‐term
impact
SARS‐CoV‐2
infection
on
bone
continues
to
pose
new
challenges
for
global
public
health.
In
recent
years,
numerous
animal
model
and
clinical
studies
have
revealed
severe
acute
respiratory
syndrome
coronavirus
2
(SARS‐CoV‐2)
can
lead
secondary
osteoporosis.
mechanisms
involved
are
related
virus's
direct
effects
tissue,
dysregulation
body's
inflammatory
response,
hypoxia,
noncoding
RNA
imbalance,
metabolic
abnormalities.
Although
these
unveiled
connection
between
osteoporosis,
current
research
is
not
comprehensive
in
depth.
Future
needed
evaluate
density
metabolism,
elucidate
specific
pathogenesis,
explore
potential
interventions.
This
review
aims
collate
existing
literature
infection‐induced
summarize
underlying
mechanisms,
provide
direction
future
research.
Viruses,
Год журнала:
2023,
Номер
15(12), С. 2434 - 2434
Опубликована: Дек. 15, 2023
The
COVID-19
pandemic
caused
by
the
SARS-CoV-2
(β-CoV)
betacoronavirus
has
posed
a
significant
threat
to
global
health.
Despite
availability
of
vaccines,
virus
continues
spread,
and
there
is
need
for
alternative
strategies
alleviate
its
impact.
Vitamin
D,
secosteroid
hormone
best
known
role
in
bone
health,
exhibits
immunomodulatory
effects
certain
viral
infections.
Here,
we
have
shown
that
bioactive
vitamin
D
(calcitriol)
limits
vitro
replication
murine
coronaviruses
MHV-3
MHV-A59.
Comparative
studies
involving
wild-type
mice
intranasally
infected
with
MHV-3,
model
studying
β-CoV
respiratory
infections,
confirmed
protective
effect
vivo.
Accordingly,
fed
standard
diet
rapidly
succumbed
infection,
whereas
those
on
D-rich
(10,000
IU
Journal of Medical Virology,
Год журнала:
2024,
Номер
96(4)
Опубликована: Апрель 1, 2024
Abstract
The
Coronavirus
Disease
2019
(COVID‐19)
pandemic
has
resulted
in
the
loss
of
millions
lives,
although
a
majority
those
infected
have
managed
to
survive.
Consequently,
set
outcomes,
identified
as
long
COVID,
is
now
emerging.
While
primary
target
severe
acute
respiratory
syndrome
coronavirus
2
(SARS‐CoV‐2)
system,
impact
COVID‐19
extends
various
body
parts,
including
bone.
This
study
aims
investigate
effects
SARS‐CoV‐2
infection
on
osteoclastogenesis,
utilizing
both
ancestral
and
Omicron
viral
strains.
Monocyte‐derived
macrophages,
which
serve
precursors
osteoclasts,
were
exposed
variants.
However,
proved
abortive,
even
though
ACE2
receptor
expression
increased
postinfection,
with
no
significant
cellular
viability
redox
balance.
Both
strains
heightened
osteoclast
formation
dose‐dependent
manner,
well
CD51/61
bone
resorptive
ability.
Notably,
induced
early
pro‐inflammatory
M1
macrophage
polarization,
shifting
toward
an
M2‐like
profile.
Osteoclastogenesis‐related
genes
(RANK,
NFATc1,
DC‐STAMP,
MMP9)
upregulated,
surprisingly,
variants
promoted
RANKL‐independent
formation.
thorough
investigation
illuminates
intricate
interplay
between
precursors,
suggesting
potential
implications
for
homeostasis
opening
new
avenues
therapeutic
exploration
COVID‐19.
Angiogenesis-osteogenesis
coupling
is
critical
for
proper
functioning
and
maintaining
the
health
of
bones.
Any
disruption
in
this
coupling,
associated
with
aging
disease,
might
lead
to
loss
bone
mass.
Osteoporosis
(OP)
a
debilitating
metabolic
disorder
that
affects
microarchitecture
bones,
gradually
leading
fracture.
Computational
analysis
revealed
normal
angiogenesis
disrupted
during
progression
OP,
especially
postmenopausal
osteoporosis
(PMOP).
The
genes
OP
PMOP
were
retrieved
from
DisGeNET
database.
Hub
gene
molecular
pathway
enrichment
performed
via
Cytoscape
plugins
STRING,
MCODE,
CytoHubba,
ClueGO
web-based
tool
Enrichr.
Twenty-eight
(28)
hub
identified,
eight
which
transcription
factors
(HIF1A,
JUN,
TP53,
ESR1,
MYC,
PPARG,
RUNX2
SOX9).
Analysis
SNPs
gnomAD,
I-Mutant2.0,
MUpro,
ConSurf
COACH
servers
substitution
F201L
IL6
as
most
deleterious.
protein
was
modeled
SWISS-MODEL
server
analyzed
YASARA
FoldX
plugin.
A
positive
ΔΔG
(1.936)
mutant
indicates
mutated
structure
less
stable
than
wild-type
is.
Thirteen
genes,
including
enriched
pathways
found
be
profoundly
involved
angiogenesis/endothelial
function
immune
signaling.
Mechanical
loading
bones
through
weight-bearing
exercises
can
activate
osteoblasts
mechanotransduction
increased
formation.
present
study
suggests
mechanical
preventive
strategy
PMOP,
by
status
maintained.
This
silico
could
used
understand
etiology
develop
novel
therapeutic
approaches.