Biomedicines,
Journal Year:
2024,
Volume and Issue:
12(10), P. 2279 - 2279
Published: Oct. 8, 2024
:
Damage
to
renal
tubular
cells
(RTCs)
represents
a
critical
pathological
manifestation
in
calcium
oxalate
(CaOx)
stone
disease,
but
the
underlying
mechanism
remains
elusive.
Energy
metabolism
reprogramming
is
vital
influencer
of
RTC
survival,
and
SMYD2
histone
methylation
transferase
that
has
been
extensively
implicated
various
metabolic
disorders.
Hence,
this
research
aimed
identify
whether
induces
energy
RTCs
exposed
CaOx
nephrolithiasis.
Frontiers in Physiology,
Journal Year:
2024,
Volume and Issue:
14
Published: Jan. 12, 2024
Kidney
injury
and
repair
are
accompanied
by
significant
disruptions
in
metabolic
pathways,
leading
to
renal
cell
dysfunction
further
contributing
the
progression
of
pathology.
This
review
outlines
complex
involvement
various
energy
production
pathways
glucose,
lipid,
amino
acid,
ketone
body
metabolism
within
kidney.
We
provide
a
comprehensive
summary
aberrant
regulation
these
kidney
repair.
After
acute
(AKI),
there
is
notable
mitochondrial
damage
oxygen/nutrient
deprivation,
reduced
activity
glycolysis
bioenergetics.
Additionally,
occur
pentose
phosphate
pathway
(PPP),
acid
metabolism,
supply
bodies.
The
subsequent
phase
characterized
shift
toward
glycolysis,
along
with
decreased
fatty
β-oxidation
continued
disturbances
metabolism.
Furthermore,
impact
on
injury,
regeneration,
development
fibrosis
analyzed.
Finally,
we
discuss
potential
therapeutic
strategies
targeting
ameliorate
promote
Advanced Science,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 4, 2025
Abstract
The
incidence
of
kidney
stones
is
increasing
worldwide.
However,
the
underlying
mechanism
process
stone
formation
and
damage
caused
are
not
well
understood.
Here,
it
observed
that
Lgals3,
a
β‐galactoside‐binding
protein,
significantly
increased
in
tissues
with
calcium
oxalate
(CaOx)
stones,
both
vivo
vitro
models.
Lgals3
expression
positively
correlated
deposition
CaOx
crystals.
Knockout
markedly
reduces
crystal
renal
fibrosis
vivo.
Furthermore,
deficiency
decrease
glycolytic
rate
lactate
production
during
inhibited
histone
lactylation
H3K18la.
Mechanistic
studies
shows
directly
interacted
key
glycolysis
protein
pyruvate
kinase
M2
(PKM2)
promoted
its
by
modulating
E3
ligase
Trim21,
preventing
ubiquitination
PKM2.
H3K18
injury
vitro.
inhibites
transcription,
activation,
FGFR4
through
inhibition
These
findings
suggest
may
play
role
interacting
PKM2
promoting
H3K18la‐mediated
gene
transcription
activation.
Frontiers in Physiology,
Journal Year:
2024,
Volume and Issue:
15
Published: Jan. 19, 2024
Sepsis-associated
acute
kidney
injury
presents
as
a
critical
condition
characterized
by
prolonged
hospital
stays,
elevated
mortality
rates,
and
an
increased
likelihood
of
transition
to
chronic
disease.
suppresses
fatty
acid
oxidation
oxidative
phosphorylation
in
the
mitochondria
renal
tubular
epithelial
cells,
thus
favoring
metabolic
shift
towards
glycolysis
for
energy
production.
This
acts
protective
mechanism
kidneys.
However,
extended
reliance
on
may
contribute
atrophy,
fibrosis,
subsequent
disease
progression.
Metabolic
reprogramming
interventions
have
emerged
prospective
strategies
counteract
sepsis-associated
restoring
normal
function,
offering
potential
therapeutic
preventive
modalities.
review
delves
into
alterations
cells
associated
with
injury,
stressing
importance
immune
response
urgency
normalization.
We
present
various
intervention
targets
that
could
facilitate
recovery
phosphorylation-centric
metabolism.
These
novel
insights
aim
transform
clinical
prevention
treatment
landscape
focus
mechanisms.
investigation
provide
valuable
clinicians
aiming
enhance
patient
outcomes
context
injury.
Advanced Science,
Journal Year:
2024,
Volume and Issue:
11(40)
Published: Aug. 9, 2024
Abstract
Epigenetic
regulation
of
metabolism
profoundly
influences
cell
fate
commitment.
During
osteoclast
differentiation,
the
activation
RANK
signaling
is
accompanied
by
metabolic
reprogramming,
but
epigenetic
mechanisms
which
induces
this
reprogramming
remain
elusive.
By
transcriptional
sequence
and
ATAC
analysis,
study
identifies
that
upregulates
PRMT6
modification,
triggering
a
switching
from
fatty
acids
oxidation
toward
glycolysis.
Conversely,
Prmt6
deficiency
reverses
shift,
markedly
reducing
HIF‐1α‐mediated
glycolysis
enhancing
acid
oxidation.
Consequently,
or
inhibitor
impedes
differentiation
alleviates
bone
loss
in
ovariectomized
(OVX)
mice.
At
molecular
level,
reduces
asymmetric
dimethylation
H3R2
at
promoters
genes
including
Ppard
,
Acox3
Cpt1a
genomic
accessibility
for
thus
emerges
as
checkpoint,
mediating
switch
to
glycolysis,
thereby
supporting
osteoclastogenesis.
Unveiling
PRMT6's
critical
role
epigenetically
orchestrating
shifts
osteoclastogenesis
offers
promising
target
anti‐resorptive
therapy.