Histone deacetylases and their inhibitors in inflammatory diseases
Sen-Yu Zhang,
No information about this author
Liying Zhang,
No information about this author
Ri Wen
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et al.
Biomedicine & Pharmacotherapy,
Journal Year:
2024,
Volume and Issue:
179, P. 117295 - 117295
Published: Aug. 14, 2024
Despite
considerable
research
efforts,
inflammatory
diseases
remain
a
heavy
burden
on
human
health,
causing
significant
economic
losses
annually.
Histone
deacetylases
(HDACs)
play
role
in
regulating
inflammation
(via
histone
and
non-histone
protein
deacetylation)
chromatin
structure
gene
expression
regulation.
Herein,
we
present
detailed
description
of
the
different
HDACs
their
functions
analyze
diseases,
including
pro-inflammatory
cytokine
production
reduction,
immune
cell
function
modulation,
anti-inflammatory
activity
enhancement.
Although
HDAC
inhibitors
have
shown
broad
disease
treatment
potentials,
clinical
applicability
remains
limited
because
non-specific
effects,
adverse
drug
resistance.
With
further
insight,
these
are
expected
to
become
important
tools
for
wide
range
diseases.
This
review
aims
explore
mechanisms
application
prospects
multiple
Language: Английский
Role of malate dehydrogenase 1 and isocitrate dehydrogenase 1 and their posttranslational modifications in diseases
Chunxia Shi,
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Yukun Wang,
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Jin Guo
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et al.
Biochemical and Biophysical Research Communications,
Journal Year:
2025,
Volume and Issue:
754, P. 151535 - 151535
Published: Feb. 24, 2025
Language: Английский
Embryonic lethal abnormal vision like 1-stabilized histone deacetylase 6 promotes hepatic stellate cell activation to accelerate liver fibrosis progression through ribosomal protein S5 downregulation
CytoJournal,
Journal Year:
2025,
Volume and Issue:
22, P. 30 - 30
Published: March 6, 2025
Histone
deacetylase
6
(HDAC6)
has
been
confirmed
to
participate
in
the
regulation
of
liver
fibrosis
(LF)
progression.
This
study
aims
explore
role
and
mechanism
HDAC6
LF
process.
Serum
samples
were
collected
from
cirrhosis
(LC)
patients
normal
healthy
individuals.
Human
hepatic
stellate
cells
(HSC;
LX-2)
stimulated
with
transforming
growth
factor
β1
(TGF-β1)
mimic
cell
models.
The
levels
HDAC6,
ribosomal
protein
S5
(RPS5),
embryonic
lethal
abnormal
vision
like
1
(ELAVL1),
fibrosis-related
markers
determined
by
quantitative
real-time
polymerase
chain
reaction
or
western
blot.
Cell
proliferation
invasion
detected
using
counting
kit
8
assay,
5-ethynyl-2'-deoxyuridine
Transwell
assay.
contents
inflammatory
factors
examined
enzyme-linked
immunosorbent
Furthermore,
co-immunoprecipitation
RNA
immunoprecipitation
assays
performed
assess
interaction
between
RPS5
ELAVL1.
effect
ELAVL1
knockdown
on
mRNA
stability
was
evaluated
Actinomycin
D
treatment
showed
increased
expression
LC
patients.
reduced
TGF-β1-induced
LX-2
proliferation,
invasion,
fibrosis,
inflammation.
Moreover,
acetylation
RPS5,
reversed
inhibition
si-HDAC6
Meanwhile,
interacted
stabilize
its
mRNA,
thus
inhibiting
expression.
Our
data
revealed
that
ELAVL1-stabilized
promoted
HSC
activation
repressing
acetylation,
providing
a
novel
target
for
alleviating
Language: Английский
The Roles of White Adipose Tissue and Liver NADPH in Dietary Restriction-Induced Longevity
Leah E. Jamerson,
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Patrick C. Bradshaw
No information about this author
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(7), P. 820 - 820
Published: July 8, 2024
Dietary
restriction
(DR)
protocols
frequently
employ
intermittent
fasting.
Following
a
period
of
fasting,
meal
consumption
increases
lipogenic
gene
expression,
including
that
NADPH-generating
enzymes
fuel
lipogenesis
in
white
adipose
tissue
(WAT)
through
the
induction
transcriptional
regulators
SREBP-1c
and
CHREBP.
knockout
mice,
unlike
controls,
did
not
show
an
extended
lifespan
on
DR
diet.
WAT
cytoplasmic
NADPH
is
generated
by
both
malic
enzyme
1
(ME1)
pentose
phosphate
pathway
(PPP),
while
liver
primarily
synthesized
folate
cycle
provided
one-carbon
units
serine
catabolism.
During
daily
fasting
diet,
fatty
acids
are
released
from
transported
to
peripheral
tissues,
where
they
used
for
beta-oxidation
phospholipid
lipid
droplet
synthesis,
monounsaturated
(MUFAs)
may
activate
Nrf1
inhibit
ferroptosis
promote
longevity.
Decreased
PPP
stimulated
browning
protected
high-fat
high
levels
macrophages
linked
obesity.
But
oscillations
[NADPH]/[NADP+]
feeding
cycles
play
important
role
maintaining
metabolic
plasticity
drive
Studies
measuring
malate/pyruvate
as
proxy
[NADPH]/[NADP+],
well
studies
using
fluorescent
biosensors
expressed
animal
models
monitor
changes
needed
during
ad
libitum
diets
determine
associated
with
Language: Английский