Clinical Cosmetic and Investigational Dermatology,
Год журнала:
2025,
Номер
Volume 18, С. 677 - 686
Опубликована: Март 1, 2025
The
aging
of
skin
has
important
impact
on
various
systems,
and
certain
(SG)
markers
can
not
only
help
with
early
diagnosis,
but
also
provide
new
ideas
for
pathophysiological
research
treatment
strategies.
To
identify
target
genes
related
to
SG
through
bioinformatics
technology
anti-aging.
Differential
expression
(DEGs)
were
screened
transcriptome
information
from
GEO
datasets
(GSE85358
GSE670988).
Based
eQTL
GWAS
datasets,
Mendelian
Randomization
(MR)
analysis
was
applied
associations
between
gene
SG.
Then,
(AS-IGs)
obtained
based
above
two
steps,
functional
pathway
analyses
performed
explore
the
potential
mechanisms
AS-IGs
in
Finally,
CIBERSORT
evaluation
used
assess
infiltration
immune
cells
Seven
selected
intersection
612
DEGs
399
genes.
enrichment
results
showed
there
60
GO
terms
may
involved
process
SG,
like
fatty-acyl-CoA
metabolic
process,
while
KEGG
pathways
identified
mainly
fatty
acid
metabolism,
energy
generation,
inflammation
regulation.
that
NK
resting
main
infiltrating
cells.
play
roles
body.
These
molecules
involve
multiple
systems
body,
such
as
function,
neuroendocrine
function.
Cellular and Molecular Life Sciences,
Год журнала:
2022,
Номер
79(5)
Опубликована: Апрель 16, 2022
Abstract
Bile
acids
are
soluble
derivatives
of
cholesterol
produced
in
the
liver
that
subsequently
undergo
bacterial
transformation
yielding
a
diverse
array
metabolites.
The
bulk
bile
acid
synthesis
takes
place
primary
acids;
however,
other
tissues
have
also
capacity
to
generate
(e.g.
ovaries).
Hepatic
then
transported
and
released
into
intestines.
In
large
intestine,
fraction
is
converted
secondary
by
gut
bacteria.
majority
intestinal
reuptake
return
liver.
A
small
remains
circulation
exert
receptor-mediated
pure
chemical
effects
acidic
oesophageal
cancer)
on
cancer
cells.
this
review,
we
assess
how
changes
biosynthesis,
flux
local
concentration
modulate
behavior
different
cancers.
Here,
present
in-depth
involvement
oesophageal,
gastric,
hepatocellular,
pancreatic,
colorectal,
breast,
prostate,
ovarian
cancer.
Previous
studies
often
used
supraphysiological
concentration,
sometimes
concentrations
1000
times
higher
than
highest
reported
tissue
or
serum
likely
eliciting
unspecific
effects,
practice
advocate
against
review.
Furthermore,
show
that,
although
were
classically
considered
as
pro-carcinogenic
agents
cancer),
dogma
switch,
lower
correspond
their
reference
possess
anticancer
activity
subset
Differences
response
cancers
lie
differential
expression
receptors
between
FXR
vs.
TGR5).
UDCA,
sold
generic
medication
cholestasis
biliary
surge,
its
conjugates
identified
with
almost
purely
features
suggesting
possibility
for
drug
repurposing.
Taken
together,
tumor
inducers
promoter
molecules;
nevertheless,
certain
cancers,
like
breast
cancer,
may
act
suppressors
Janus-faced
nature
carcinogenesis.
Summary
Chronic
inflammation
of
adipose
tissue
is
a
prominent
characteristic
many
metabolic
diseases.
Lipid
metabolism
in
consistently
dysregulated
during
inflammation,
which
characterized
by
substantial
infiltration
proinflammatory
cells
and
high
cytokine
concentrations.
Adipose
caused
variety
endogenous
factors,
such
as
mitochondrial
dysfunction,
reactive
oxygen
species
(ROS)
production,
endoplasmic
reticulum
(ER)
stress,
cellular
senescence,
ceramides
biosynthesis
mediators
lipopolysaccharides
(LPS)
signaling.
Additionally,
the
gut
microbiota
also
plays
crucial
role
regulating
inflammation.
Essentially,
arises
from
an
imbalance
adipocyte
regulation
immune
cells.
Specific
inflammatory
signals,
including
nuclear
factor‐κB
(NF‐κB)
signaling,
inflammasome
signaling
inflammation‐mediated
autophagy,
have
been
shown
to
be
involved
regulation.
The
pathogenesis
diseases
chronic
(obesity,
insulin
resistance,
atherosclerosis
nonalcoholic
fatty
liver
disease
[NAFLD])
recent
research
regarding
potential
therapeutic
targets
for
these
conditions
are
discussed
this
review.
Expert Reviews in Molecular Medicine,
Год журнала:
2024,
Номер
26
Опубликована: Янв. 1, 2024
Abstract
PARP2,
that
belongs
to
the
family
of
ADP-ribosyl
transferase
enzymes
(ART),
is
a
discovery
millennium,
as
it
was
identified
in
1999.
Although
PARP2
described
initially
DNA
repair
factor,
now
evident
partakes
regulation
or
execution
multiple
biological
processes
inflammation,
carcinogenesis
and
cancer
progression,
metabolism
oxidative
stress-related
diseases.
Hereby,
we
review
involvement
these
with
aim
understanding
which
are
specific
for
but
not
other
members
ART
family.
A
better
functions
all
crucial
development
new
PARP-centred
selective
therapies.
Abstract
ADP-ribosylation
is
a
post-translational
modification
involved
in
variety
of
processes
including
DNA
damage
repair,
transcriptional
regulation,
and
cellular
proliferation.
Depending
on
the
number
ADP
moieties
transferred
to
target
proteins,
can
be
classified
either
as
mono-ADP-ribosylation
(MARylation)
or
poly-ADP-ribosylation
(PARylation).
This
catalyzed
by
enzymes
known
ADP-ribosyltransferases
(ARTs),
which
include
poly
(ADP-ribose)-polymerase
(PARP)
superfamily
proteins.
Certain
members
PARP
family
PARP1
PARP2
have
been
extensively
studied
assessed
therapeutic
targets.
However,
other
protein
are
not
well
but
gained
attention
recent
years
given
findings
suggesting
their
roles
an
increasing
processes.
Among
these
PARP10
PARP14,
gradually
emerged
key
players
maintenance
genomic
stability
carcinogenesis.
PARP14
catalyze
transfer
single
moiety
Here,
we
summarize
current
knowledge
MARylation
repair
cancer,
focusing
PARP14.
We
highlight
cancer
progression
response
chemotherapeutics
briefly
discuss
currently
inhibitors.
BMC Pharmacology and Toxicology,
Год журнала:
2024,
Номер
25(1)
Опубликована: Янв. 3, 2024
Abstract
Background
To
comprehend
the
influences
of
fenofibrate
on
hepatic
lipid
accumulation
and
mitochondrial
function-related
signaling
pathways
in
mice
with
non-alcoholic
fatty
liver
disease
(NAFLD)
secondary
to
high-fat
diets
together
free
acids-influenced
HepG2
cells
model.
Materials
methods
A
random
allocation
male
6-week
C57BL/6J
into
three
groups
was
done,
including
controls,
model
(14
weeks
a
diet),
[similar
one
administered
0.04
g/(kg.d)
by
gavage
at
11
for
4
weeks]
groups,
which
contained
10
each.
This
study
verified
NAFLD
pathogenesis
via
functions
pathological
abnormalities,
index
weight,
body
serum
biochemical
indexes,
oxidative
stress
indicators,
function
related
pathways.
The
effect
intervention
investigated
mice.
In
vitro,
four
based
were
generated,
FFA
(1.5
mmol/L
incubation
24
h),
LV-PGC-1α
(similar
after
PPARGC1A
lentivirus
transfection),
LV
control
negative
transfection)
groups.
mechanism
PGC-1α
decomposition
biosynthesis
Oil
red
O
staining,
colorimetry
western
blot.
Results
vivo
experiments,
diet
achieved
remarkable
changes
regarding
index,
changes,
weight
while
improved
objective
indicators.
model,
increased
significantly
within
group,
aggravated
hepatocytic
damage
boosted
levels.
Moreover,
induced
excessive
mitosis
fragmented
morphology,
ATP
content
decreased,
mtDNA
replication
fold
expression
protein
PPARα
reduced,
PGC-1α,
NRF-1
TFAM
decreased.
overexpression
inhibited
deposition
improving
decomposition.
Conclusion
Fenofibrate
up-regulated
PPARα/PGC-1α
pathway,
promoted
β-oxidation,
reduced
liver.
enhanced
production,
intracellular
lipids
stress.
