Epigenetic
aging
clocks
represent
contemporary
biomarkers
that
predict
age
using
methylomic
data.
These
models
can
be
categorized
as
first-generation
estimate
chronological
or
next-generation
are
designed
to
associate
with
health,
lifestyle,
and/or
outcomes.
Recently,
we
created
a
buccal
clock
called
CheekAge
associates
all-cause
mortality
risk
in
older
adults.
To
better
understand
our
model,
collated
25
Infinium
MethylationEPIC
datasets
the
Gene
Expression
Omnibus
database
and
analyzed
ability
of
five
other
well-known
distinct
health
disease
signals.
outcompeted
every
tested
by
significantly
associating
total
33
different
variables,
including
human
immunodeficiency
virus,
major
depressive
disorder,
psychological
trauma,
prediabetes,
body
mass
index,
non-alcoholic
fatty
liver
disease,
pulmonary
fibrosis,
exposure
chemical
endocrine
disruptor
PBB-153,
various
cancers
tumors.
Of
six
tested,
outperformed
clocks.
underlying
biology
CheekAge,
iteratively
removed
CpG
inputs
identify
DNA
methylation
sites
promoted
antagonized
each
association.
Finally,
performed
detailed
enrichment
analyses
on
these
unveil
overrepresented
biological
processes
transcription
factor
targets.
Trends in Molecular Medicine,
Год журнала:
2024,
Номер
30(6), С. 592 - 604
Опубликована: Апрель 10, 2024
Pancreatic
ductal
adenocarcinoma
(PDAC)
is
a
highly
aggressive
form
of
pancreatic
cancer,
known
for
its
challenging
diagnosis
and
limited
treatment
options.
The
focus
on
metabolic
reprogramming
as
key
factor
in
tumor
initiation,
progression,
therapy
resistance
has
gained
prominence.
In
this
review
we
the
impact
changes
interplay
among
stromal,
immune,
cells,
glutamine
branched-chain
amino
acids
(BCAAs)
emerge
pivotal
players
modulating
immune
cell
functions
growth.
We
also
discuss
ongoing
clinical
trials
that
explore
modulation
PDAC,
targeting
mitochondrial
metabolism,
asparagine
addiction,
autophagy
inhibition.
Overcoming
challenges
understanding
nutrient
effects
immune-stromal-tumor
interactions
holds
promise
innovative
therapeutic
strategies.
Abstract
Diabesity
is
a
condition
where
an
individual
has
both
diabetes
and
obesity,
which
can
lead
to
severe
complications
including
cardiovascular
disease,
leading
cause
of
mortality.
Recently,
cancer
become
excess
hospitalizations,
obesity
are
associated
with
higher
risk
developing
several
types
cancer.
In
this
review,
we
propose
that
chronic
stress
significantly
increases
association.
Managing
challenging
as
they
significant
distress.
The
relationship
between
interconnected,
anxiety
depression
being
common
in
patients.
Cancer
diagnosis
treatment
lasting
changes
the
body’s
neuroendocrine
system,
causing
excessive
release
catecholamines
prostaglandins
patients
undergoing
surgery,
promotes
spread
other
parts
body.
Furthermore,
could
increase
diabetes,
or
both.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(13), С. 7175 - 7175
Опубликована: Июнь 29, 2024
Obesity
is
a
global
health
challenge
that
has
received
increasing
attention
in
contemporary
research.
The
gut
microbiota
been
implicated
the
development
of
obesity,
primarily
through
its
involvement
regulating
various
host
metabolic
processes.
Recent
research
suggests
epigenetic
modifications
may
serve
as
crucial
pathways
which
and
metabolites
contribute
to
pathogenesis
obesity
other
disorders.
Hence,
understanding
interplay
between
mechanisms
for
elucidating
impact
on
host.
This
review
focuses
relationship
with
several
obesity-related
pathogenic
mechanisms,
including
energy
dysregulation,
inflammation,
maternal
inheritance.
These
findings
could
novel
therapeutic
targets
probiotics,
prebiotics,
fecal
transplantation
tools
treating
disruptions.
It
also
aid
developing
strategies
modulate
microbiota,
thereby
characteristics
obesity.
Abstract
The
importance
of
vitamin
D
for
a
well-functioning
immune
system
is
becoming
increasingly
evident.
Nevertheless,
the
other
fat-soluble
vitamins
A,
E
and
K
also
seem
to
play
central
role
regarding
adequate
function
cells
counteract
excessive
reactions
inflammatory
processes.
However,
recognizing
hidden
hunger,
particularly
micronutrient
deficiencies
in
vulnerable
groups
like
elderly,
crucial
because
older
adults
often
lack
sufficient
micronutrients
various
reasons.
This
review
summarizes
latest
findings
on
modulating
functions
physiological
pathophysiological
context,
provides
graphical
comparison
Recommended
Daily
Allowances
between
Deutschland,
Austria,
Confoederatio
Helvetica
(D-A-CH;
eng.
GSA,
Germany,
Switzerland,
Austria),
Deutsche
Gesellschaft
für
Ernährung
(DGE;
German
Nutrition
Society)
National
Institutes
Health
(NIH)
across
all
age
and,
particular,
addresses
question
benefits
supplementation
respective
aging
population
industrialized
nations
strengthen
system.
following
highlights
D,
which
critical
roles
maintaining
some
cases,
preventing
activation.
Therefore,
better
understanding
relevance
blood
levels
consequently
potential
strategies
may
contribute
prevention
management
infectious
diseases
as
well
overall
health
elderly.
Journal of Hepatology,
Год журнала:
2025,
Номер
unknown
Опубликована: Март 1, 2025
The
liver
acts
as
a
central
metabolic
hub,
integrating
signals
from
the
gastrointestinal
tract
and
adipose
tissue
to
regulate
carbohydrate,
lipid,
amino
acid
metabolism.
Gut-derived
metabolites,
such
acetate
ethanol
non-esterified
fatty
acids
white
(WAT),
influence
hepatic
processes,
which
rely
on
mitochondrial
function
maintain
systemic
energy
balance.
Metabolic
dysregulation
obesity,
insulin
resistance,
type
2
diabetes
disrupt
these
pathways,
leading
dysfunction-associated
steatotic
disease
(MASLD)
steatohepatitis
(MASH).
This
review
explores
fluxes
within
gut-adipose
tissue-liver
axis,
focusing
pivotal
role
of
de
novo
lipogenesis
(DNL),
dietary
substrates
like
glucose
fructose,
changes
in
during
MASLD
progression.
It
highlights
contributions
resistance
impaired
dynamics
lipid
accumulation.
Further
understanding
how
interplay
between
substrate
flux
gastro-intestinal
integrates
with
intersects
structural
functional
alterations
mitochondria
will
be
important
identify
novel
therapeutic
targets
advance
treatment
MASH.
Cell Reports,
Год журнала:
2024,
Номер
43(8), С. 114636 - 114636
Опубликована: Авг. 1, 2024
Inflammatory
bowel
disease
(IBD)
has
high
prevalence
in
Western
counties.
The
fat
content
diets
is
one
of
the
leading
causes
for
this
prevalence;
however,
underlying
mechanisms
have
not
been
fully
defined.
Here,
we
find
that
high-fat
diet
(HFD)
induces
ferroptosis
intestinal
regulatory
T
(Treg)
cells,
which
might
be
key
initiating
step
disruption
immunotolerance
and
development
colitis.
Compared
with
effector
Treg
cells
favor
lipid
metabolism
prefer
polyunsaturated
fatty
acids
(PUFAs)
synthesis
membrane
phospholipids.
Therefore,
consumption
HFD,
PUFAs
such
as
arachidonic
acid,
cultivates
vulnerable
Tregs
are
fragile
to
peroxidation
ferroptosis.
Treg-cell-specific
deficiency
GPX4,
enzyme
maintaining
cellular
redox
homeostasis
preventing
ferroptosis,
dramatically
aggravates
pathogenesis
HFD-induced
IBD.
Taken
together,
these
studies
expand
our
understanding
IBD
etiology.
Cellular and Molecular Immunology,
Год журнала:
2024,
Номер
unknown
Опубликована: Дек. 10, 2024
While
immunotherapy
with
immune
checkpoint
inhibitors
(ICIs)
has
revolutionized
the
clinical
management
of
various
malignancies,
a
large
fraction
patients
are
refractory
to
ICIs
employed
as
standalone
therapeutics,
necessitating
development
combinatorial
treatment
strategies.
Immunogenic
cell
death
(ICD)
inducers
have
attracted
considerable
interest
partners
for
ICIs,
at
least
in
part
owing
their
ability
initiate
tumor-targeting
adaptive
response.
However,
compared
either
approach
alone,
regimens
involving
ICD
and
not
always
shown
superior
activity.
Here,
we
discuss
accumulating
evidence
on
therapeutic
interactions
between
oncological
settings,
identify
key
factors
that
may
explain
discrepancies
preclinical
findings,
propose
strategies
address
existing
challenges
increase
efficacy
these
combinations
cancer.
Ferroptosis
is
characterized
as
an
iron-dependent
and
lipophilic
form
of
cell
death.
However,
it
remains
unclear
what
role
ferroptosis
has
in
adipose
tissue
function
activity.
Here,
we
find
a
lower
ferroptotic
signature
the
individuals
mice
with
obesity.
We
further
that
activation
signaling
by
non-lethal
dose
agonists
significantly
reduces
lipid
accumulation
primary
adipocytes
high-fat
diet
(HFD)-fed
mice.
Notably,
adipocyte-specific
overexpression
acyl-coenzyme
A
synthetase
long-chain
family
member
4
(Acsl4)
or
deletion
ferritin
heavy
chain
(Fth)
protects
from
HFD-induced
expansion
metabolic
disorders
via
signaling.
Mechanistically,
5,15-dihydroxyeicosatetraenoic
acid
(5,15-DiHETE)
activates
signaling,
resulting
degradation
hypoxia-inducible
factor-1α
(HIF1α),
thereby
derepressing
thermogenic
program
regulated
c-Myc-peroxisome
proliferator-activated
receptor
gamma
coactivator-1
beta
(Pgc1β)
pathway.
Our
findings
suggest
activating
tissues
might
help
to
prevent
treat
obesity
its
related
disorders.
