Frontiers in Physiology,
Journal Year:
2019,
Volume and Issue:
10
Published: Dec. 18, 2019
Growing
elderly
populations
are
an
increasingly
serious
health
and
socio-economic
concern
for
modern
societies.
Science
has
made
tremendous
progress
in
the
understanding
of
aging
itself
which
somehow
helped
medicine
to
extend
life
expectancies.
With
increase
expectancy,
incidence
chronic
age-related
diseases
(ARDs)
also
increased.
A
new
approach
trying
solve
this
problem
is
concept
geroscience.
This
implies
that
process
common
cause
all
ARDs.
The
corollary
consequence
such
thinking
we
can
should
treat
itself.
How
move
into
medical
practice
a
big
challenge,
but
if
consider
as
disease
solved.
However,
there
no
definition
what
is,
its
causes
are,
why
it
occurs,
target(s)
interventions
be,
impossible
definitively
conclude
disease.
On
contrary,
may
be
strongly
considered
not
treated;
nonetheless,
likely
amenable
optimization
changes/adaptations
at
individual
level
achieve
better
functional
healthspan.
Abstract
In
recent
years,
the
focus
on
human
inflammation
in
research
has
increased,
with
aging-related
widely
recognized
as
a
defining
characteristic
of
aging.
Inflammation
is
strongly
correlated
mitochondrial
dysfunction.
Phosphoglycerate
mutase
family
member
5
(PGAM5)
novel
modulator
homeostasis
response
to
mechanical
stimulation.
Here
we
review
structure
and
sublocalization
PGAM5,
introduce
its
importance
programmed
cell
death
summarize
crucial
roles
development
progression
inflammatory
diseases
such
pneumonia,
hepatitis,
neuroinflammation
Notably,
PGAM5
dual
effects
controlling
inflammation:
distinct
PGAM5-mediated
functions
exhibit
cellular
heterogeneity,
leading
control.
We
therefore
highlight
double-edged
sword
nature
potential
critical
regulator
innovative
therapeutic
target
inflammation.
Finally,
challenges
future
directions
use
which
properties,
molecule
clinic
are
discussed.
This
provides
insights
guide
intelligent
strategies
targeting
PGAM5-specific
regulation
treat
intractable
conditions,
well
extension
broader
application
other
achieve
more
precise
effective
treatment
outcomes.
Proceedings of the National Academy of Sciences,
Journal Year:
2020,
Volume and Issue:
117(35), P. 21519 - 21526
Published: Aug. 17, 2020
The
intestinal
epithelium
is
a
highly
dynamic
structure
that
rejuvenates
in
response
to
acute
stressors
and
can
undergo
alterations
cellular
composition
as
animals
age.
microbiota,
acting
via
secreted
factors
related
indole,
appear
regulate
the
sensitivity
of
promote
epithelial
repair
IL-22
type
I
IFN
signaling.
As
age,
changes,
resulting
decreased
proportion
goblet
cells
colon.
We
show
colonization
young
or
geriatric
mice
with
bacteria
secrete
indoles
various
derivatives
administration
indole
derivative
indole-3
aldehyde
increases
proliferation
promotes
cell
differentiation,
reversing
an
effect
aging.
To
induce
acts
xenobiotic
aryl
hydrocarbon
receptor
increase
expression
cytokine
IL-10.
However,
effects
on
do
not
depend
signaling,
pathways
responsible
for
protection
against
stressors.
Thus,
derived
from
commensal
microbiota
homeostasis,
especially
during
aging,
mechanisms
distinct
those
used
responses
Indoles
may
have
utility
intervention
limit
decline
barrier
integrity
systemic
inflammation
occurs
Biomedicines,
Journal Year:
2020,
Volume and Issue:
8(7), P. 198 - 198
Published: July 7, 2020
People
exposed
to
chronic
stress
age
rapidly.
The
telomeres
in
their
cells
of
all
types
shorten
faster.
Inflammation
is
another
important
feature
that,
along
with
aging,
accounts
for
the
phenomenon
inflammaging.
In
addition
aging
itself,
inflammaging
can
contribute
development
several
pathologies,
including
atherosclerosis,
diabetes,
hypertension,
and
others.
Oxidative
one
main
mechanisms
related
stress.
caused
by
over-production
reactive
oxygen
species
(ROS)
that
damage
various
tissues.
source
ROS
mitochondria.
Being
suppressed
mitochondrial
mutations,
mitophagy
aggravate
situation.
this
case,
aging-specific
pro-inflammatory
changes
are
amplified.
It
happens
because
inability
maintain
normal
state
Macrophages
crucial
element
innate
immunity
associated
inflammation
and,
subsequently,
review,
we
focus
on
therapy
approaches
potentially
reducing
deleterious
effects
oxidative
These
include
stimulation
mitophagy,
activation
uncoupling,
induction
expression
telomerase
catalytic
component
gene,
use
antioxidants.
Any
method
should
improve
post-traumatic
disorder.
Journal of Molecular Medicine,
Journal Year:
2020,
Volume and Issue:
99(1), P. 1 - 20
Published: Oct. 6, 2020
Abstract
Chronic
low-grade
inflammation
is
a
common
hallmark
of
the
aging
process
and
many
age-related
diseases.
There
substantial
evidence
that
persistent
associated
with
compensatory
anti-inflammatory
response
which
prevents
excessive
tissue
damage.
Interestingly,
inflammatory
state
encountered
aging,
called
inflammaging,
anti-inflammaging
process.
The
activation
immunosuppressive
network
includes
an
increase
in
numbers
myeloid-derived
suppressor
cells
(MDSC),
regulatory
T
(Treg),
macrophages
(Mreg/M2c).
Immunosuppressive
secrete
several
cytokines,
e.g.,
TGF-β
IL-10,
as
well
reactive
oxygen
nitrogen
species
(ROS/RNS).
Moreover,
suppress
function
effector
immune
by
catabolizing
l
-arginine
tryptophan
through
arginase
1
(ARG1)
indoleamine
2,3-dioxygenase
(IDO),
respectively.
Unfortunately,
armament
also
induces
harmful
bystander
effects
neighboring
impairing
host
homeostasis.
For
instance,
signaling
can
trigger
degenerative
changes,
cellular
senescence,
fibrosis,
osteoporosis,
muscle
atrophy,
degeneration
extracellular
matrix.
In
addition,
changes
levels
ROS,
RNS,
metabolites
kynurenine
pathway
impair
This
review
will
examine
detail
on
tissues.
It
seems
this
immunosuppression
damage
but
promotes
Key
messages
•
Low-grade
Persistent
activates
aging.
mechanisms
evoke
Immunosuppression
Cells,
Journal Year:
2021,
Volume and Issue:
10(11), P. 2974 - 2974
Published: Nov. 1, 2021
Aging
is
the
result
of
deterioration
homeostatic
systems
(nervous,
endocrine,
and
immune
systems),
which
preserve
organism’s
health.
We
propose
that
age-related
impairment
these
due
to
establishment
a
chronic
oxidative
stress
situation
leads
low-grade
inflammation
throughout
system’s
activity.
It
known
system
weakens
with
age,
increases
morbidity
mortality.
In
this
context,
we
describe
how
function
cells
can
be
used
as
an
indicator
rate
aging
individual.
addition
passive
role
marker,
work
driver
by
amplifying
oxidative-inflammatory
associated
(oxi-inflamm-aging)
inducing
senescence
in
far
tissue
cells.
Further
supporting
our
theory,
discuss
certain
lifestyle
conditions
(such
social
environment,
nutrition,
or
exercise)
have
impact
on
longevity
affecting
inflammatory
state
cells,
regulating
immunosenescence
its
contribution
oxi-inflamm-aging.
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
23(7), P. 3785 - 3785
Published: March 29, 2022
The
brain
is
one
of
the
most
energy-consuming
organs
in
body.
Satisfying
such
energy
demand
requires
compartmentalized,
cell-specific
metabolic
processes,
known
to
be
complementary
and
intimately
coupled.
Thus,
relies
on
thoroughly
orchestrated
energy-obtaining
agents,
processes
molecular
features,
as
neurovascular
unit,
astrocyte–neuron
coupling,
cellular
distribution
substrate
transporters.
Importantly,
early
features
aging
process
are
determined
by
progressive
perturbation
certain
responsible
for
adequate
supply,
resulting
hypometabolism.
These
age-related
alterations
further
worsened
during
prodromal
stages
neurodegenerative
diseases,
namely
Alzheimer’s
disease
(AD),
preceding
onset
clinical
symptoms,
anatomically
functionally
associated
with
loss
cognitive
abilities.
Here,
we
focus
concrete
neuroenergetic
brain’s
fueling
glucose
lactate,
transporters
vascular
system
guaranteeing
its
interactions
between
astrocytes
neurons,
neurodegenerative-related
disruption.
We
sought
review
principles
underlying
dimension
healthy
AD
brains,
suggest
that
integration
these
concepts
preventive,
diagnostic
treatment
strategies
key
improving
precision
interventions.
Vaccines,
Journal Year:
2022,
Volume and Issue:
10(4), P. 607 - 607
Published: April 13, 2022
Organismal
ageing
is
associated
with
many
physiological
changes,
including
differences
in
the
immune
system
of
most
animals.
These
are
often
considered
to
be
a
key
cause
age-associated
diseases
as
well
decreased
vaccine
responses
humans.
The
cited
failure
seasonal
influenza,
but,
while
it
usually
case
that
efficiency
this
lower
older
than
younger
adults,
not
always
true,
and
reasons
for
differential
manifold.
Undoubtedly,
changes
innate
adaptive
response
respond
influenza
vaccine,
but
unclear.
Moreover,
recent
advances
formulations
adjuvants,
our
understanding
ageing,
have
contributed
development
vaccines,
such
those
against
herpes
zoster
SARS-CoV-2,
can
protect
serious
disease
adults
just
people.
In
present
article,
we
discuss
why
myth
vaccines
inevitably
less
individuals,
represent
one
powerful
means
health
ensure
quality
life
adults.
