Egyptian Academic Journal of Biological Sciences. C, Physiology and Molecular Biology/Egyptian Academic Journal of Biological Sciences. C, Physiology and Molecular Biology,
Journal Year:
2023,
Volume and Issue:
15(2), P. 215 - 229
Published: Sept. 5, 2023
Folic
acid,
Red
blood
cells
(RBCs),
White
(WBCs)
and
platelets
(PLTs).Leukemia
is
a
type
of
cancer
that
develops
in
the
bone
marrow
cells.When
DNA
cell
undergoes
one
mutation
or
series
mutations
results
formation
leukemia
cells.These
cells,
"blasts,"
cannot
mature
into
fully
functioning
WBCs.Leukemia
increases
WBCs
which
compete
for
space
with
RBCs
body
requires
to
function
normally;
each
may
be
classified
as
acute
chronic,
myeloid
lymphoid,
depending
on
originating
growth
rate.Nearly
2.5%
all
new
cases
3.1%
cancer-related
deaths
were
attributable
Leukemia.Leukemia
can
strike
at
any
age
geographical
ethnic
differences
rates
are
also
present.Folate's
significance
was
exclusively
tied
antifolate-based
treatment.After
discovering
Antifolate
associated
based
chemotherapy,
contrary
inhibitory
action
antifolate
tumors,
epidemiologic,
clinical,
experimental
data
show
folate
deficiency
normal
tissues
predispose
them
neoplastic
transformation
supplementation
suppress
development
tumors
tissues.Epidemiologic
research
reveals
negative
connection
between
levels
numerous
cancers,
including
Leukemia.The
exact
association
status
certain
cancers
unknown.Vitamin
B
control
one-carbon
metabolism
human
health.Folatemediated
carbon
(1C)
supports
processes
essential
cell.Through
number
interlinked
reactions
happening
cytosol
mitochondria
cell,
contributes
de
novo
purine
thymidylate
synthesis,
methionine
cycle
redox
defense.Targeting
gave
rise
modern
chemotherapy.The
cycles
complete
route
vitamin
B9
folate.Vitamin
B6
regulates
cycling.Vitamin
dysregulation
alters
biochemical
signaling
causes
several
illnesses.
Epigenetics & Chromatin,
Journal Year:
2025,
Volume and Issue:
18(1)
Published: March 29, 2025
Macrophage
polarization
is
a
dynamic
process
driven
by
complex
interplay
of
cytokine
signaling,
metabolism,
and
epigenetic
modifications
mediated
pathogens.
Upon
encountering
specific
environmental
cues,
monocytes
differentiate
into
macrophages,
adopting
either
pro-inflammatory
(M1)
or
anti-inflammatory
(M2)
phenotype,
depending
on
the
cytokines
present.
M1
macrophages
are
induced
interferon-gamma
(IFN-γ)
characterized
their
reliance
glycolysis
role
in
host
defense.
In
contrast,
M2
stimulated
interleukin-4
(IL-4)
interleukin-13
(IL-13),
favor
oxidative
phosphorylation
participate
tissue
repair
responses.
Metabolism
tightly
linked
to
regulation,
because
key
metabolic
intermediates
such
as
acetyl-coenzyme
A
(CoA),
α-ketoglutarate
(α-KG),
S-adenosylmethionine
(SAM),
nicotinamide
adenine
dinucleotide
(NAD+)
serve
cofactors
for
chromatin-modifying
enzymes,
which
turn,
directly
influences
histone
acetylation,
methylation,
RNA/DNA
protein
arginine
methylation.
These
control
gene
expression
regulating
chromatin
accessibility,
thereby
modulating
macrophage
function
polarization.
Histone
acetylation
generally
promotes
more
open
structure
conducive
activation,
while
methylation
can
activate
repress
residue
its
state.
Crosstalk
between
modifications,
further
fine-tunes
phenotypes
transcriptional
networks
response
cues.
While
primarily
functions
epigenetics
through
degradation
methylated
proteins
releases
derivatives
like
asymmetric
dimethylarginine
(ADMA),
contribute
metabolism-a
factor
This
review
explores
intricate
relationships
metabolism
regulation
during
better
understanding
this
crosstalk
will
likely
generate
novel
therapeutic
insights
manipulating
infections
tuberculosis
inflammatory
diseases
diabetes.
Translational Psychiatry,
Journal Year:
2022,
Volume and Issue:
12(1)
Published: Nov. 17, 2022
Abstract
Impaired
cognition
is
often
overlooked
in
the
clinical
management
of
depression,
despite
its
association
with
poor
psychosocial
functioning
and
reduced
engagement.
There
an
outstanding
need
for
new
treatments
to
address
this
unmet
need,
highlighted
by
our
consultations
individuals
lived
experience
depression.
Here
we
consider
evidence
support
different
pharmacological
approaches
treatment
impaired
including
that
influence
primary
neurotransmission
directly
as
well
novel
targets
such
neurosteroid
modulation.
We
also
potential
methodological
challenges
establishing
a
strong
base
area,
disentangle
direct
effects
on
from
more
generalised
symptomatic
improvement
identification
sensitive,
reliable
objective
measures
cognition.
Cell Death and Differentiation,
Journal Year:
2024,
Volume and Issue:
31(5), P. 558 - 573
Published: April 3, 2024
Esophageal
squamous
cell
carcinoma
(ESCC)
is
a
deadly
malignancy
with
notable
metabolic
reprogramming,
yet
the
pivotal
feature
driving
ESCC
progression
remains
elusive.
Here,
we
show
that
methionine
cycle
exhibits
robust
activation
in
and
reversely
associated
patient
survival.
cells
readily
harness
exogenous
to
generate
S-adenosyl-methionine
(SAM),
thus
promoting
proliferation.
Mechanistically,
augments
METTL3-mediated
RNA
m
Nutrients,
Journal Year:
2024,
Volume and Issue:
16(12), P. 1860 - 1860
Published: June 13, 2024
Evidence
is
emerging
on
the
role
of
maternal
diet,
gut
microbiota,
and
other
lifestyle
factors
in
establishing
lifelong
health
disease,
which
are
determined
by
transgenerationally
inherited
epigenetic
modifications.
Understanding
mechanisms
may
help
identify
novel
biomarkers
for
gestation-related
exposure,
burden,
or
disease
risk.
Such
essential
developing
tools
early
detection
risk
exposure
levels.
It
necessary
to
establish
an
threshold
due
nutrient
deficiencies
environmental
that
can
result
clinically
relevant
alterations
modulate
risks
fetus.
This
narrative
review
summarizes
latest
updates
roles
nutrients
(n-3
fatty
acids,
polyphenols,
vitamins)
microbiota
placental
epigenome
its
impacts
fetal
brain
development.
unravels
potential
functional
targeted
intervention
ensure
optimal
development
performance
later
life.
Cell Death and Disease,
Journal Year:
2025,
Volume and Issue:
16(1)
Published: March 18, 2025
Abstract
Cardiovascular
diseases
are
the
leading
causes
of
death
worldwide.
However,
there
still
shortcomings
in
currently
employed
treatment
methods
for
these
diseases.
Therefore,
exploring
molecular
mechanisms
underlying
cardiovascular
is
an
important
avenue
developing
new
strategies.
Previous
studies
have
confirmed
that
metabolic
and
epigenetic
alterations
often
involved
across
patients.
Moreover,
factors
interact
with
each
other
affect
progression
a
coordinated
manner.
Lactylation
novel
posttranslational
modification
(PTM)
links
metabolism
epigenetics
affects
disease
progression.
analyzing
crosstalk
between
cellular
expected
to
provide
insights
development
The
purpose
this
review
describe
relationship
heart
such
as
failure,
myocardial
infarction,
atherosclerosis,
focus
on
acylation
methylation,
propose
potential
therapeutic
measures.
ABSTRACT
Transfer
RNA
(tRNA)
is
not
merely
a
passive
carrier
of
amino
acids,
but
an
active
regulator
mRNA
translation
controlling
codon
bias
and
optimality.
The
synthesis
various
tRNA
modifications
regulated
by
many
“writer”
enzymes,
which
utilize
substrates
from
metabolic
pathways
or
dietary
sources.
Metabolic
bioenergetic
pathways,
such
as
one‐carbon
(1C)
metabolism
the
tricarboxylic
acid
(TCA)
cycle
produce
essential
for
synthesis,
S‐Adenosyl
methionine
(SAM),
sulfur
species,
α‐ketoglutarate
(α‐KG).
activity
these
can
directly
impact
decoding
via
regulating
levels.
In
this
review,
we
discuss
complex
interactions
between
diet,
metabolism,
modifications,
translation.
We
how
nutrient
availability,
bioenergetics,
intermediates
modulate
modification
landscape
to
fine‐tune
protein
synthesis.
Moreover,
highlight
dysregulation
metabolic‐tRNA
contributes
disease
pathogenesis,
including
cancer,
disorders,
neurodegenerative
diseases.
also
new
emerging
field
GlycoRNA
biology
drawing
parallels
glycobiology
diseases
guide
future
directions
in
area.
Throughout
our
discussion,
links
specific
their
metabolic/dietary
precursors,
diseases,
emphasizing
importance
metabolism‐centric
view
understanding
pathologies.
Future
research
should
focus
on
uncovering
interplay
cellular
contexts.
Addressing
gaps
will
into
novel
interventions.