Abstract
Sleep
deficiency
is
associated
with
obesity,
but
the
mechanisms
underlying
this
connection
remain
unclear.
Here,
we
identify
a
sleep-inducible
hypothalamic
protein
hormone
in
humans
and
mice
that
suppresses
obesity.
This
cleaved
from
reticulocalbin-2
(RCN2),
name
it
Raptin.
Raptin
release
timed
by
circuit
vasopressin-expressing
neurons
suprachiasmatic
nucleus
to
RCN2-positive
paraventricular
nucleus.
levels
peak
during
sleep,
which
blunted
sleep
deficiency.
binds
glutamate
metabotropic
receptor
3
(GRM3)
of
hypothalamus
stomach
inhibit
appetite
gastric
emptying,
respectively.
Raptin-GRM3
signaling
mediates
anorexigenic
effects
via
PI3K-AKT
signaling.
Of
note,
verify
connections
between
deficiencies
sleeping
state,
impaired
release,
obesity
patients
Moreover,
carrying
an
RCN2
nonsense
variant
present
night
eating
syndrome
These
data
define
unique
food
intake
prevents
With
aging,
there
is
increased
dysfunction
of
both
innate
and
adaptive
immune
responses,
which
contributes
to
impaired
responses
pathogens
greater
mortality
morbidity.
This
age-related
defined
in
general
as
immunosenescence
includes
an
increase
the
number
memory
T
cells,
loss
ability
respond
antigen
a
lingering
level
low-grade
inflammation.
However,
certain
features
are
similar
cellular
senescence,
irreversible
proliferation
response
damage
stress.
Importantly,
senescence
cells
can
develop
inflammatory
senescence-associated
secretory
phenotype
(SASP),
that
also
drives
non-autonomous
dysfunction.
Interestingly,
viral
infection
extent
directly
indirectly,
leading
inflammation,
especially
elderly.
review
focuses
on
dysfunction,
pathogens.
The
gut
microbiota
(GM)
plays
a
crucial
role
in
maintaining
the
overall
health
and
well-being
of
host.
Recent
studies
have
demonstrated
that
GM
may
significantly
influence
bone
metabolism
degenerative
skeletal
diseases,
such
as
osteoporosis
(OP).
Interventions
targeting
modification,
including
probiotics
or
antibiotics,
been
found
to
affect
remodeling.
This
review
provides
comprehensive
summary
recent
research
on
regulating
remodeling
seeks
elucidate
regulatory
mechanism
from
various
perspectives,
interaction
with
immune
system,
interplay
estrogen
parathyroid
hormone
(PTH),
impact
metabolites,
effect
extracellular
vesicles
(EVs).
Moreover,
this
explores
potential
therapeutic
approach
for
OP.
insights
presented
contribute
development
innovative
GM-targeted
therapies
International Journal of Molecular Sciences,
Год журнала:
2022,
Номер
23(5), С. 2701 - 2701
Опубликована: Фев. 28, 2022
Age-related
chronic
diseases
are
an
enormous
burden
to
modern
societies
worldwide.
Among
these,
osteoporosis,
a
condition
that
predisposes
individuals
increased
risk
of
fractures,
substantially
contributes
mortality
and
health-care
costs
in
elderly.
It
is
now
well
accepted
advanced
chronical
age
one
the
main
factors
for
diseases.
Hence,
targeting
fundamental
aging
mechanisms
such
as
senescence
has
become
promising
option
treatment
these
Moreover,
pathophysiological
concepts
arise
from
menopause
causing
estrogen
deficiency,
aging.
Here,
we
focus
on
recent
advances
understanding
senescence-related
contributing
age-related
bone
loss.
Furthermore,
options
senile
osteoporosis
senescent
cells
reviewed.
Acta Pharmaceutica Sinica B,
Год журнала:
2024,
Номер
14(4), С. 1508 - 1524
Опубликована: Янв. 20, 2024
Macrophage
senescence,
manifested
by
the
special
form
of
durable
cell
cycle
arrest
and
chronic
low-grade
inflammation
like
senescence-associated
secretory
phenotype,
has
long
been
considered
harmful.
Persistent
senescence
macrophages
may
lead
to
maladaptation,
immune
dysfunction,
finally
development
age-related
diseases,
infections,
autoimmune
malignancies.
However,
it
is
a
ubiquitous,
multi-factorial,
dynamic
complex
phenomenon
that
also
plays
roles
in
remodeled
processes,
including
wound
repair
embryogenesis.
In
this
review,
we
summarize
some
general
molecular
changes
several
specific
biomarkers
during
macrophage
which
bring
new
sight
recognize
senescent
different
conditions.
Also,
take
an
in-depth
look
at
functional
macrophages,
metabolism,
autophagy,
polarization,
phagocytosis,
antigen
presentation,
infiltration
or
recruitment.
Furthermore,
degenerations
diseases
associated
with
as
well
mechanisms
relevant
genetic
regulations
are
integrated,
not
only
emphasizing
possibility
regulating
benefit
age-associated
but
implication
on
finding
potential
targets
drugs
clinically.
Frontiers in Endocrinology,
Год журнала:
2022,
Номер
13
Опубликована: Сен. 6, 2022
Osteoporosis
is
a
skeletal
system
disease
characterized
by
low
bone
mass
and
altered
microarchitecture,
with
an
increased
risk
of
fractures.
Classical
theories
hold
that
osteoporosis
essentially
remodeling
disorder
caused
estrogen
deficiency/aging
(primary
osteoporosis)
or
secondary
to
diseases/drugs
(secondary
osteoporosis).
However,
the
in-depth
understanding
intricate
nexus
between
both
immune
in
recent
decades,
novel
field
“Immunoporosis”
was
proposed
Srivastava
et
al.
(2018,
2022),
which
delineated
growing
importance
cells
osteoporosis.
This
review
aimed
summarize
response
(immune
inflammatory
factors)
different
types
In
postmenopausal
osteoporosis,
deficiency-mediated
alteration
stimulates
activation
osteoclasts
varying
degrees.
senile
aging
contributes
continuous
at
level
breaks
balance,
ultimately
resulting
loss.
Further
diabetic
insulin
deficiency
resistance-induced
hyperglycemia
could
lead
abnormal
regulation
cells,
excessive
production
proinflammatory
factors,
Thus,
we
reviewed
pathophysiology
from
insight-immunoporosis,
expected
provide
specific
therapeutic
target
for
