Aging Cell,
Journal Year:
2019,
Volume and Issue:
18(6)
Published: Sept. 27, 2019
Abstract
An
emerging
body
of
data
suggests
that
lipid
metabolism
has
an
important
role
to
play
in
the
aging
process.
Indeed,
a
plethora
dietary,
pharmacological,
genetic,
and
surgical
lipid‐related
interventions
extend
lifespan
nematodes,
fruit
flies,
mice,
rats.
For
example,
impairment
genes
involved
ceramide
sphingolipid
synthesis
extends
both
worms
flies.
The
overexpression
fatty
acid
amide
hydrolase
or
lysosomal
lipase
prolongs
life
Caenorhabditis
elegans
,
while
diacylglycerol
enhances
longevity
C.
Drosophila
melanogaster
.
removal
adipose
tissue
rats,
increased
expression
apolipoprotein
D
survival
flies
mice.
Mouse
can
be
additionally
extended
by
genetic
deletion
acyltransferase
1,
treatment
with
steroid
17‐α‐estradiol,
ketogenic
diet.
Moreover,
phospholipase
A2
receptor
improves
various
healthspan
parameters
progeria
mouse
model.
Genome‐wide
association
studies
have
found
several
variants
associated
human
aging.
epsilon
2
4
alleles
E
are
extreme
late‐onset
neurodegenerative
disease,
respectively.
In
humans,
blood
triglyceride
levels
tend
increase,
lysophosphatidylcholine
decrease
age.
Specific
phospholipid
profiles
also
been
shown
change
age
exceptional
longevity.
These
suggest
may
improve
lipids
likely
represent
rich
source
biomarkers.
FEBS Journal,
Journal Year:
2020,
Volume and Issue:
287(16), P. 3350 - 3369
Published: April 7, 2020
The
inflammatory
response
involves
the
activation
of
several
cell
types
to
fight
insults
caused
by
a
plethora
agents,
and
maintain
tissue
homoeostasis.
On
one
hand,
cells
involved
in
pro‐inflammatory
response,
such
as
M1
macrophages,
Th1
Th17
lymphocytes
or
activated
microglia,
must
rapidly
provide
energy
fuel
inflammation,
which
is
essentially
accomplished
glycolysis
high
lactate
production.
other
regulatory
T
M2
are
immune
regulation
resolution
preferentially
use
fatty
acid
oxidation
through
TCA
cycle
main
source
for
Here,
we
discuss
impact
glycolytic
metabolism
at
different
steps
response.
Finally,
review
wide
variety
molecular
mechanisms
could
explain
relationship
between
metabolites
phenotype,
including
signalling
events,
epigenetic
remodelling,
post‐transcriptional
post‐translational
modifications.
Inflammatory
processes
common
feature
many
age‐associated
diseases,
cardiovascular
neurodegenerative
disorders.
finding
that
immunometabolism
be
master
regulator
inflammation
broadens
avenue
treating
inflammation‐related
pathologies
manipulation
vascular
metabolism.
Circulation Research,
Journal Year:
2016,
Volume and Issue:
118(10), P. 1563 - 1576
Published: May 12, 2016
The
aging
population
is
increasing
in
developed
countries.
Because
the
incidence
of
cardiac
disease
increases
dramatically
with
age,
it
important
to
understand
molecular
mechanisms
through
which
heart
becomes
either
more
or
less
susceptible
stress.
Cardiac
characterized
by
presence
hypertrophy,
fibrosis,
and
accumulation
misfolded
proteins
dysfunctional
mitochondria.
Macroautophagy
(hereafter
referred
as
autophagy)
a
lysosome-dependent
bulk
degradation
mechanism
that
essential
for
intracellular
protein
organelle
quality
control.
Autophagy
autophagic
flux
are
generally
decreased
hearts,
murine
autophagy
loss-of-function
models
develop
exacerbated
dysfunction
accompanied
organelles.
On
contrary,
stimulation
improves
function
mouse
aggregation
removing
accumulated
proteins,
mitochondria,
damaged
DNA,
thereby
improving
overall
cellular
environment
alleviating
aging-associated
pathology
heart.
Increasing
lines
evidence
suggest
required
many
mediate
lifespan
extension,
such
caloric
restriction,
various
organisms.
These
results
raise
exciting
possibility
may
play
an
role
combating
adverse
effects
In
this
review,
we
discuss
during
aging,
how
alleviates
age-dependent
changes
heart,
level
can
be
restored.
Proceedings of the National Academy of Sciences,
Journal Year:
2018,
Volume and Issue:
115(8)
Published: Feb. 5, 2018
Emerging
findings
suggest
that
compromised
cellular
bioenergetics
and
DNA
repair
contribute
to
the
pathogenesis
of
Alzheimer's
disease
(AD),
but
their
role
in
disease-defining
pathology
is
unclear.
We
developed
a
repair-deficient
3xTgAD/Polβ
Aging Cell,
Journal Year:
2019,
Volume and Issue:
18(6)
Published: Sept. 27, 2019
Abstract
An
emerging
body
of
data
suggests
that
lipid
metabolism
has
an
important
role
to
play
in
the
aging
process.
Indeed,
a
plethora
dietary,
pharmacological,
genetic,
and
surgical
lipid‐related
interventions
extend
lifespan
nematodes,
fruit
flies,
mice,
rats.
For
example,
impairment
genes
involved
ceramide
sphingolipid
synthesis
extends
both
worms
flies.
The
overexpression
fatty
acid
amide
hydrolase
or
lysosomal
lipase
prolongs
life
Caenorhabditis
elegans
,
while
diacylglycerol
enhances
longevity
C.
Drosophila
melanogaster
.
removal
adipose
tissue
rats,
increased
expression
apolipoprotein
D
survival
flies
mice.
Mouse
can
be
additionally
extended
by
genetic
deletion
acyltransferase
1,
treatment
with
steroid
17‐α‐estradiol,
ketogenic
diet.
Moreover,
phospholipase
A2
receptor
improves
various
healthspan
parameters
progeria
mouse
model.
Genome‐wide
association
studies
have
found
several
variants
associated
human
aging.
epsilon
2
4
alleles
E
are
extreme
late‐onset
neurodegenerative
disease,
respectively.
In
humans,
blood
triglyceride
levels
tend
increase,
lysophosphatidylcholine
decrease
age.
Specific
phospholipid
profiles
also
been
shown
change
age
exceptional
longevity.
These
suggest
may
improve
lipids
likely
represent
rich
source
biomarkers.
