Colorimetric and fluorescent dual-modality assay for cell-free mitochondrial DNA copy number in saliva
Jiaxu Wang,
No information about this author
Zheng‐Rong Lu,
No information about this author
Zhanmin Liu
No information about this author
et al.
Analytical Biochemistry,
Journal Year:
2025,
Volume and Issue:
unknown, P. 115840 - 115840
Published: March 1, 2025
Language: Английский
A positive association between high dietary medium-chain fatty acids intake and depression: Mediation of inflammation
Journal of Affective Disorders,
Journal Year:
2025,
Volume and Issue:
unknown
Published: April 1, 2025
Language: Английский
A novel LGALS1-depended and immune-associated fatty acid metabolism risk model in acute myeloid leukemia stem cells
Huanhuan Qin,
No information about this author
Meixi Peng,
No information about this author
Jingsong Cheng
No information about this author
et al.
Cell Death and Disease,
Journal Year:
2024,
Volume and Issue:
15(7)
Published: July 5, 2024
Leukemia
stem
cells
(LSCs)
are
recognized
as
the
root
cause
of
leukemia
initiation,
relapse,
and
drug
resistance.
Lipid
species
highly
abundant
essential
component
human
cells,
which
often
changed
in
tumor
microenvironment.
LSCs
remodel
lipid
metabolism
to
sustain
stemness.
However,
there
is
no
useful
related
biomarker
has
been
approved
for
clinical
practice
AML
prediction
treatment.
Here,
we
constructed
verified
fatty
acid
metabolism-related
risk
score
(LFMRS)
model
based
on
TCGA
database
via
a
series
bioinformatics
analysis,
univariate
COX
regression
multivariate
found
that
LFMRS
could
be
an
independent
factor
predict
survival
time
patients
combined
with
age.
Moreover,
revealed
Galectin-1
(LGALS1,
key
gene
LFMRS)
was
expressed
associated
poor
prognosis
patients,
LGALS1
repression
inhibited
cell
LSC
proliferation,
enhanced
apoptosis,
decreased
accumulation
vitro.
curbed
progression,
accumulation,
CD8
Language: Английский
Comparative proteomic analysis of renal tissue of normotensive and hypertensive rats
О.А. Бунеева,
No information about this author
V.I. Fedchenko,
No information about this author
S.A. Kaloshina
No information about this author
et al.
Biomeditsinskaya Khimiya,
Journal Year:
2024,
Volume and Issue:
70(2), P. 89 - 98
Published: Jan. 1, 2024
Comparative
proteomic
analysis
of
kidney
tissue
from
normotensive
(WKY)
and
spontaneously
hypertensive
(SHR)
rats
revealed
quantitative
qualitative
changes
in
renal
proteins.
The
number
proteins
specific
for
WKY
(blood
pressure
110–120
mm
Hg)
was
13–16.
There
were
20–24
SHR
180
Hg
more).
total
identified
common
both
rat
strains
included
972–975
A
pairwise
comparison
all
possible
(SHR-WKY)
variants
8
only
animals,
7
ones
(SHR).
Taking
into
consideration
their
biological
roles,
the
lack
some
enzyme
(for
example,
biliverdin
reductase
A)
reduces
production
molecules
exhibiting
antihypertensive
properties,
while
appearance
others
(e.g.
betaine-homocysteine
S-methyltransferase
2,
septin
etc.)
can
be
interpreted
as
a
compensatory
reaction.
Renal
with
altered
relative
content
(with
more
than
2.5-fold
change)
accounted
no
5%
Among
an
increased
largest
group
consisted
involved
processes
energy
generation
carbohydrate
metabolism,
well
antioxidant
protective
In
context
development
hypertension,
apparently
considered
compensatory.
most
pronounced
decrease
rats,
dramatic
reduction
acyl-CoA
medium-chain
synthetase-3
(ACSM3)
appears
to
make
important
contribution
pathology
these
animals.
Language: Английский
MAPK signaling pathway induced LOX-1+ polymorphonuclear myeloid-derived suppressor cells in biliary atresia
Cheng Chen,
No information about this author
Hezhen Wang,
No information about this author
Lili Xu
No information about this author
et al.
Clinical Immunology,
Journal Year:
2024,
Volume and Issue:
268, P. 110355 - 110355
Published: Sept. 3, 2024
Language: Английский
Proteomics exploration of metformin hydrochloride for diabetic kidney disease treatment via the butanoate metabolism pathway
Jiyun Chai,
No information about this author
Yan Wang,
No information about this author
Sifan Guo
No information about this author
et al.
Journal of Pharmaceutical and Biomedical Analysis,
Journal Year:
2024,
Volume and Issue:
254, P. 116584 - 116584
Published: Nov. 26, 2024
Language: Английский
Chewing the fat for good health: ACSM3 deficiency exacerbates metabolic syndrome
The EMBO Journal,
Journal Year:
2024,
Volume and Issue:
43(4), P. 481 - 483
Published: Jan. 23, 2024
The
origin
of
metabolic
syndrome,
a
pathophysiological
condition
facilitating
cardiovascular
disease,
diabetes,
and
other
comorbidities,
remains
poorly
understood.
Recent
work
by
Xiao
et
al
(2023)
identifies
the
mitochondrial
enzyme
ACSM3
as
determinant
lipid
homeostasis
hepatic
health
in
mice
patients.
Additionally,
authors
identified
deleterious
downstream
p38-MAPK
signalling
targetable
feature
deficiency
that
may
help
to
ameliorate
syndrome.
Language: Английский
Mitochondrial dysfunction and onset of type 2 diabetes along with its complications: a multi-omics Mendelian randomization and colocalization study
Yang Li,
No information about this author
Yahu Miao,
No information about this author
Qing Feng
No information about this author
et al.
Frontiers in Endocrinology,
Journal Year:
2024,
Volume and Issue:
15
Published: Aug. 30, 2024
Mitochondrial
dysfunction
plays
a
crucial
role
in
Type
2
Diabetes
Mellitus
(T2DM)
and
its
complications.
However,
the
genetic
pathophysiology
remains
under
investigation.
Through
multi-omics
Mendelian
Randomization
(MR)
colocalization
analyses,
we
identified
mitochondrial-related
genes
causally
linked
with
T2DM
Language: Английский