Nutrients,
Journal Year:
2024,
Volume and Issue:
16(7), P. 946 - 946
Published: March 26, 2024
Recently,
we
reported
that
during
the
hypertrophic
phase
(230
days
old)
of
hereditary
cardiomyopathy
hamster
(HCMH),
short-term
treatment
(20
days)
with
250
mg/kg/day
taurine
prevents
development
hypertrophy
in
males
but
not
females.
However,
mortality
rate
non-treated
animals
was
higher
females
than
males.
To
verify
whether
sex-dependency
effect
is
due
to
difference
disease’s
progression,
treated
230-day-old
for
a
longer
time
period
122
days.
Our
results
showed
long-term
low
and
high
concentrations
significantly
cardiac
early
death
HCMH
(p
<
0.0001
p
0.05,
respectively)
0.01
0.0001,
respectively).
demonstrate
sex
dependency
treatments
degree
heart
remodeling
when
compared
dependency.
In
addition,
studies
should
consider
differences
between
male
female
progression
disease.
Thus,
therapies
are
recommended
prevent
cardiomyopathy.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(6), P. 3298 - 3298
Published: March 14, 2024
The
identification
of
pathological
links
among
metabolic
disorders,
kidney
ailments,
and
cardiovascular
conditions
has
given
rise
to
the
concept
cardiovascular–kidney–metabolic
(CKM)
syndrome.
Emerging
prenatal
risk
factors
seem
increase
likelihood
CKM
syndrome
across
an
individual’s
lifespan.
renin–angiotensin
system
(RAS)
plays
a
crucial
role
in
maternal–fetal
health
maintaining
homeostasis
cardiovascular,
metabolic,
functions.
This
review
consolidates
current
preclinical
evidence
detailing
how
dysregulation
RAS
during
pregnancy
lactation
leads
characteristics
offspring,
elucidating
underlying
mechanisms.
multi-organ
effects
RAS,
influencing
fetal
programming
triggering
traits
suggest
it
as
promising
reprogramming
strategy.
Additionally,
we
present
overview
interventions
targeting
prevent
traits.
comprehensive
potential
early-life
aims
expedite
clinical
translation
process,
ultimately
enhancing
outcomes
health.
Biomedicines,
Journal Year:
2025,
Volume and Issue:
13(2), P. 452 - 452
Published: Feb. 12, 2025
Cardiovascular-kidney-metabolic
syndrome
(CKMS)
has
become
a
significant
global
health
challenge.
Since
CKMS
often
originates
early
in
life,
as
outlined
by
the
developmental
origins
of
and
disease
(DOHaD)
concept,
prevention
is
more
effective
strategy
than
treatment.
Various
animal
models,
classified
environmental
exposures
or
mechanisms,
are
used
to
explore
CKMS.
However,
no
single
model
can
fully
replicate
all
aspects
its
clinical
stages,
limiting
advancement
preventive
therapeutic
strategies.
This
review
aims
assist
researchers
comparing
strengths
limitations
common
models
programming
studies
highlighting
key
considerations
for
selecting
suitable
models.
Nutrients,
Journal Year:
2024,
Volume and Issue:
16(9), P. 1263 - 1263
Published: April 24, 2024
Amino
acids
are
essential
for
normal
pregnancy
and
fetal
development.
Disruptions
in
maternal
amino
acid
metabolism
have
been
associated
with
various
adult
diseases
later
life,
a
phenomenon
referred
to
as
the
developmental
origins
of
health
disease
(DOHaD).
In
this
review,
we
examine
recent
evidence
highlighting
significant
impact
on
programming,
their
influence
modulation
gut
microbiota,
repercussions
offspring
outcomes,
particularly
context
cardiovascular–kidney–metabolic
(CKM)
syndrome.
Furthermore,
delve
into
experimental
studies
that
unveiled
protective
effects
therapies
targeting
acids.
These
interventions
demonstrated
potential
reprogram
traits
CKM
offspring.
The
discussion
encompasses
challenges
translating
findings
from
animal
clinical
applications,
emphasizing
complexity
process.
Additionally,
propose
solutions
overcome
these
challenges.
Ultimately,
move
forward,
future
research
endeavors
should
aim
pinpoint
most
effective
amino-acid-targeted
therapies,
determining
optimal
dosage
mode
administration.
This
exploration
is
maximizing
reprogramming
effects,
ultimately
contributing
enhancement
Nutrients,
Journal Year:
2025,
Volume and Issue:
17(6), P. 995 - 995
Published: March 12, 2025
The
benefits
of
breastfeeding
for
both
mother
and
infant
are
generally
recognized;
however,
the
connections
between
breast
milk,
lactation,
long-term
offspring
health
disease
remain
incompletely
understood.
Cardiovascular–kidney–metabolic
syndrome
(CKMS)
has
become
a
major
global
public
challenge.
Insufficient
milk
supply,
combined
with
various
early-life
environmental
factors,
markedly
increases
future
risk
CKMS,
as
highlighted
by
developmental
origins
(DOHaD)
concept.
Given
its
richness
in
nutrients
bioactive
components
essential
health,
this
review
focuses
on
reprogramming
strategies
involving
to
improve
offspring’s
cardiovascular,
kidney,
metabolic
health.
It
also
highlights
recent
experimental
advances
understanding
mechanisms
driving
CKMS
programming.
Cumulatively,
evidence
suggests
that
lactational
impairment
heightens
development.
In
contrast,
early
interventions
during
lactation
period
focused
animal
models
leverage
response
cues
show
potential
improving
outcomes—an
area
warranting
further
investigation
clinical
translation.
Nitric Oxide,
Journal Year:
2025,
Volume and Issue:
unknown
Published: March 1, 2025
Sulfur-containing
amino
acids
are
involved
in
the
regulation
of
vascular
activity
and
blood
pressure.
Clinically,
a
positive
correlation
was
found
between
serum
homocysteine
levels
On
other
hand,
methionine
cysteine
were
reduced
hypertensive
patients.
Recently,
redox
state
sulfur-containing
has
emerged
as
potential
diagnostic
marker
cardiovascular
health.
Metabolomic
studies
have
revealed
shift
thiol/disulfide
ratio
toward
oxidized
forms
overproduction
thiyl
radicals
Although
accumulating
evidence
confirms
that
essential
for
maintaining
homeostasis
pressure
control,
their
hypotensive
antioxidant
properties
been
primarily
demonstrated
animal
studies.
While
several
groups
developing
new
targeted
triggered
sulfur-based
donors,
standardized
pharmacological
interventions
patients
largely
absent
pose
challenge
future
research.
In
this
review,
we
summarize
recent
investigate
role
redox-active
metabolites,
including
glutathione
sulfide,
control
development
systemic
hypertension.
Nutrients,
Journal Year:
2024,
Volume and Issue:
16(5), P. 745 - 745
Published: March 5, 2024
Endocardial
endothelium
(EE)
is
a
layer
of
cells
covering
the
cardiac
cavities
and
modulates
cardiomyocyte
function.
This
cell
type
releases
several
cardioactive
factors,
including
Angiotensin
II
(Ang
II).
octopeptide
known
to
induce
hypertrophy.
However,
whether
this
circulating
factor
also
induces
EE
hypertrophy
not
known.
Taurine
prevent
Whether
endogenous
antioxidant
prevents
effect
Ang
on
human
(hEE)
will
be
verified.
Using
quantitative
fluorescent
probe
imaging
for
calcium
reactive
oxygen
species
(ROS),
our
results
show
that
(10-7
M,
48
h
treatment)
an
increase
in
hEE
(hEEC)
volume
its
nucleus.
Pretreatment
with
20
mM
taurine
morphological
remodeling
increases
intracellular
ROS.
These
suggest
reported
associated
hEEC
later
prevented
by
reducing
ROS
overloads.
Thus,
could
excellent
tool
preventing
II-induced
hEECs.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(18), P. 9788 - 9788
Published: Sept. 10, 2024
Dietary
regulation
has
been
recognized
for
its
profound
impact
on
human
health.
The
convergence
of
cardiovascular,
kidney,
and
metabolic
disorders
at
the
pathophysiological
level
given
rise
to
cardiovascular-kidney-metabolic
(CKM)
syndrome,
which
constitutes
a
significant
global
health
burden.
Maternal
dietary
nutrients
play
crucial
role
in
fetal
development,
influencing
various
programmed
processes.
This
review
emphasizes
effects
different
types
interventions
each
component
CKM
syndrome
both
preclinical
clinical
settings.
We
also
provide
an
overview
potential
maternal
strategies,
including
amino
acid
supplementation,
lipid-associated
diets,
micronutrients,
gut
microbiota-targeted
plant
polyphenols,
aimed
preventing
offspring.
Additionally,
we
discuss
mechanisms
mediated
by
nutrient-sensing
signals
that
contribute
programming.
Altogether,
underscore
interaction
between
risk
offspring,
emphasizing
need
continued
research
facilitate
their
translation.
