Nutrients,
Journal Year:
2022,
Volume and Issue:
14(3), P. 653 - 653
Published: Feb. 3, 2022
SIRT1
is
an
NAD+-dependent
class
III
histone
deacetylase
that
abundantly
expressed
in
the
kidney,
where
it
modulates
gene
expression,
apoptosis,
energy
homeostasis,
autophagy,
acute
stress
responses,
and
mitochondrial
biogenesis.
Alterations
activity
NAD+
metabolism
are
frequently
observed
chronic
kidney
diseases
of
diverse
origins,
including
obesity
diabetes.
Nevertheless,
vitro
vivo
studies
clinical
trials
with
humans
show
SIRT1-activating
compounds
derived
from
natural
sources,
such
as
polyphenols
found
fruits,
vegetables,
plants,
resveratrol,
quercetin,
isoflavones,
can
prevent
disease
be
part
treatments
for
a
wide
variety
diseases.
Here,
we
summarize
roles
renal
pathophysiology
provide
overview
have
potential
to
restore
Frontiers in Physiology,
Journal Year:
2023,
Volume and Issue:
14
Published: Feb. 23, 2023
The
renin–angiotensin
system
(RAS)
plays
a
pivotal
role
in
blood
pressure
regulation.
In
some
cases,
this
steering
mechanism
is
affected
by
various
deleterious
factors
(mainly
via
the
overactivation
of
RAS)
causing
cardiovascular
damage,
including
coronary
heart
disease
(CHD)
that
can
ultimately
lead
to
chronic
failure
(CHF).
This
not
only
causes
disability
and
absenteeism
from
work
but
also
imposes
significant
healthcare
costs
globally.
incidence
diseases
has
escalated
exponentially
over
years
with
major
outcome
form
CHD,
stroke,
CHF.
involvement
RAS
been
extensively
researched
limelight
on
CHD.
may
trigger
cascade
events
atherosclerotic
mayhem,
which
CHD
related
aggravation
damaging
endothelial
lining
vessels
inflammatory
oxidative
stress
pathways.
Although
there
are
diagnostic
tests
treatments
available
market,
constant
need
for
development
procedures
therapeutic
strategies
increase
patient
compliance
reduce
associated
side
effects.
review
highlights
advances
treatment
domains
would
help
subjugating
effects
caused
conventional
therapy.
BMC Complementary Medicine and Therapies,
Journal Year:
2023,
Volume and Issue:
23(1)
Published: March 10, 2023
Abstract
Background
Aging
is
associated
with
impaired
renal
function
and
structural
alterations.
Oxidative
stress
plays
a
vital
role
in
senescence
damage.
Sirtuin
1
(SIRT1)
thought
to
protect
cells
from
oxidative
through
nuclear
factor
erythroid
2-related
2
(NRF2).
Ellagic
acid
(EA),
natural
antioxidant,
has
been
demonstrated
have
renoprotective
roles
vitro
vivo.
This
study
investigated
if
SIRT1
NRF2
mediate
the
protective
effects
of
EA
aged
kidneys.
Methods
Male
Wistar
rats
were
divided
into
three
groups
including
young
(4
months),
old,
old
+
(25
months).
Young
received
solvent,
while
group
was
treated
(30
mg/kg)
by
gavage
for
30
days.
Then,
level
stress,
expression,
kidney
parameters,
histopathological
indices
measured.
Results
Treatment
significantly
increased
antioxidant
enzymes
reduced
malondialdehyde
concentration
(
P
<
0.01).
Moreover,
administration
remarkably
upregulated
mRNA
protein
levels
as
well
deacetylated
0.05).
Additionally,
improved
scores
Conclusions
These
findings
suggest
that
ellagic
exerts
on
kidneys
activating
signaling.
Brain Communications,
Journal Year:
2024,
Volume and Issue:
6(2)
Published: Jan. 1, 2024
Abstract
Components
that
comprise
our
brain
parenchymal
and
cerebrovascular
structures
provide
a
homeostatic
environment
for
proper
neuronal
function
to
ensure
normal
cognition.
Cerebral
insults
(e.g.
ischaemia,
microbleeds
infection)
alter
cellular
physiologic
processes
within
the
neurovascular
unit
contribute
cognitive
dysfunction.
COVID-19
has
posed
significant
complications
during
acute
convalescent
stages
in
multiple
organ
systems,
including
brain.
Cognitive
impairment
is
prevalent
complication
patients,
irrespective
of
severity
SARS-CoV-2
infection.
Moreover,
overwhelming
evidence
from
vitro,
preclinical
clinical
studies
reported
SARS-CoV-2-induced
pathologies
components
are
associated
with
impairment.
Neurovascular
disruption
alters
coupling
response,
critical
mechanism
regulates
cerebromicrovascular
blood
flow
meet
energetic
demands
locally
active
neurons.
Normal
processing
achieved
through
response
involves
coordinated
action
cells
(i.e.
neurons
glia)
cell
types
endothelia,
smooth
muscle
pericytes).
However,
current
work
on
COVID-19-induced
yet
investigate
as
causal
factor.
Hence,
this
review,
we
aim
describe
SARS-CoV-2's
effects
how
they
can
impact
decline
disease.
Additionally,
explore
potential
therapeutic
interventions
mitigate
Given
great
both
individuals
public
health,
necessity
effort
fundamental
scientific
research
application
becomes
imperative.
This
integrated
endeavour
crucial
mitigating
deficits
induced
by
its
subsequent
burden
especially
vulnerable
population.
AJP Endocrinology and Metabolism,
Journal Year:
2020,
Volume and Issue:
319(4), P. E689 - E708
Published: Aug. 5, 2020
Much
more
serious
than
the
previous
severe
acute
respiratory
syndrome
(SARS)
coronavirus
(CoV)
outbreaks,
novel
SARS-CoV-2
infection
has
spread
speedily,
affecting
213
countries
and
causing
∼17,300,000
cases
∼672,000
(∼+1,500/day)
deaths
globally
(as
of
July
31,
2020).
The
potentially
fatal
disease
(COVID-19),
caused
by
air
droplets
airborne
as
main
transmission
modes,
clearly
induces
a
spectrum
clinical
manifestations,
but
it
also
affects
immune,
gastrointestinal,
hematological,
nervous,
renal
systems.
dramatic
scale
disorders
complications
arises
from
inadequacy
current
treatments
absence
vaccine
specific
anti-COVID-19
drugs
to
suppress
viral
replication,
inflammation,
additional
pathogenic
conditions.
This
highlights
importance
understanding
mechanisms
actions
urgent
need
prospecting
for
new
or
alternative
treatment
options.
objective
present
review
is
discuss
challenging
issue
relative
utility
plants-derived
polyphenols
in
fighting
infections.
Not
only
strong
capacity
highlighted
magnifying
health
benefits,
underlying
are
stressed.
Finally,
emphasis
placed
on
potential
ability
combat
via
regulation
its
molecular
targets
human
cellular
binding
well
through
resulting
host
oxidative
stress,
signaling
pathways.
Medical Archives,
Journal Year:
2020,
Volume and Issue:
74(2), P. 134 - 134
Published: Jan. 1, 2020
COVID-19
is
a
new
viral
illness
that
can
affect
the
lungs
and
airways
with
lethal
consequences
leading
to
death
of
patients.
The
ACE2
receptors
were
widely
disturbed
among
body
tissues
such
as
lung,
kidney,
small
intestine,
heart,
others
in
different
percent
considered
target
for
nCOVID-19
virus.
S-protein
virus
was
binding
caused
downregulation
endogenous
anti-viral
mediators,
upregulation
NF-κB
pathway,
ROS
pro-apoptotic
protein.
Nrf2
transcription
factor
that's
play
role
generation
anti-oxidant
enzymes.
Clinical Epigenetics,
Journal Year:
2020,
Volume and Issue:
12(1)
Published: Aug. 5, 2020
Abstract
Coronaviruses
(CoVs)
are
highly
diverse
single-stranded
RNA
viruses
owing
to
their
susceptibility
numerous
genomic
mutations
and
recombination.
Such
involve
human
animal
pathogens
including
the
etiologic
agents
of
acute
respiratory
tract
illnesses:
severe
syndrome
coronavirus
(SARS-CoV),
Middle
East
(MERS-CoV),
morbific
SARS-CoV-2.
Coronavirus
disease
2019
(COVID-19),
an
emerging
with
a
quick
rise
in
infected
cases
deaths,
was
recently
identified
causing
worldwide
pandemic.
COVID-19
outcomes
were
found
increase
elderly
patients
compromised
immune
system.
Evidences
indicated
that
main
culprit
behind
deaths
is
cytokine
storm,
which
illustrated
by
uncontrolled
over-production
soluble
markers
inflammation.
The
regulation
process
pathogenesis
through
molecular
mechanism
comprise
virus-host
interactions
linked
viral
entry,
replication
transcription,
escape,
system
control.
Recognizing
infections
epigenetics
lens
will
lead
potential
alteration
gene
expression
thus
limiting
infections.
Focusing
on
epigenetic
therapies
reaching
clinical
trials,
clinically
approved
epigenetic-targeted
agents,
combination
therapy
antivirals
drugs
currently
considered
effective
valuable
approach
for
inflammatory
overdrive
Oxidative Medicine and Cellular Longevity,
Journal Year:
2021,
Volume and Issue:
2021(1)
Published: Jan. 1, 2021
Podocyte
mitochondrial
dysfunction
plays
a
critical
role
in
the
pathogenesis
of
chronic
kidney
disease
(CKD).
Previous
studies
demonstrated
that
excessive
fission
could
lead
to
overproduction
reactive
oxygen
species
(ROS)
and
promote
podocyte
apoptosis.
Therefore,
maintenance
stable
function
is
newly
identified
way
protect
podocytes
prevent
progression
CKD.
As
mitochondria‐targeted
antioxidant,
mitoquinone
(MitoQ)
has
been
proven
be
promising
agent
for
prevention
injury
cardiovascular
Parkinson’s
disease.
The
present
study
examined
effects
MitoQ
on
angiotensin
II‐
(Ang
II‐)
induced
both
vivo
vitro
.
mitochondria
Ang
II‐infused
mice
exhibited
morphological
functional
alterations.
observed
fragmentation
ROS
production
were
alleviated
with
treatment.
In
,
alterations
morphology
II‐stimulated
podocytes,
including
membrane
potential
reduction,
overproduction,
adenosine
triphosphate
(ATP)
deficiency,
significantly
reversed
by
MitoQ.
Moreover,
rescued
expression
translocation
Nrf2
(nuclear
factor
E2‐related
2)
decreased
Keap1
(Kelch‐like
ECH‐associated
protein
1)
podocytes.
knockdown
partially
blocked
protective
II‐induced
oxidative
stress
These
results
demonstrate
exerts
effect
via
Keap1‐Nrf2
signaling
pathway.
Journal of Advanced Research,
Journal Year:
2021,
Volume and Issue:
41, P. 205 - 218
Published: Dec. 22, 2021
Vascular
smooth
muscle
cell
(VSMC)
senescence
in
the
vasculature
results
vascular
aging
as
well
age-related
diseases,
while
metformin
improves
inflamm-aging
profile
by
enhancing
autophagy.
However,
metformin's
impact
on
VSMC
is
largely
undefined.
To
test
hypothesis
that
exerts
an
anti-senescence
role
restoring
autophagic
activity
VSMCs
and
tissues.
Animal
models
established
angiotensin
II
(Ang
II)
induction
physiological
senescent
primary
from
aortas
of
elderly
patients
were
treated
with
metformin.
Cellular
assessed
measuring
amounts
senescence-associated
β-galactosidase
markers,
including
p21
p53.
Autophagy
levels
autophagy-related
protein
expression,
transmission
electron
microscope,
autolysosome
staining.
In
order
to
explore
underlying
mechanism
effects
metformin,
4D
label-free
quantitative
proteomics
bioinformatic
analyses
conducted,
subsequent
experiments
validating
these
findings.
Ang
II-dependent
was
suppressed
Metformin
also
significantly
improved
arterial
stiffness
alleviated
structural
changes
aged
arteries,
reduced
secretory
phenotype
(SASP),
proliferation
migration
VSMCs.
Mechanistically,
proteomic
analysis
indicated
autophagy
might
contribute
effects.
Reduced
flux
observed
II-induced
cellular
senescence;
this
reduction
reversed
Specifically,
enhanced
at
autophagosome-lysosome
fusion
level,
whereas
blockade
inhibited
prevents
promoting
formation.
Aging and Disease,
Journal Year:
2022,
Volume and Issue:
13(2), P. 468 - 468
Published: Jan. 1, 2022
Aging
and
aging-related
diseases
have
emerged
as
increasingly
severe
health
social
problems.
Therefore,
it
is
imperative
to
discover
novel
effective
therapeutics
delay
the
aging
process
manage
diseases.
Glucagon-like
peptide-1
receptor
agonists
(GLP-1
RAs),
one
of
classes
antihyperglycemic
drugs,
been
recommended
type
2
diabetes
mellitus
(T2DM).
Moreover,
GLP-1
RAs
shown
protect
against
oxidative
stress,
cellular
senescence
chronic
inflammation,
which
are
widely
accepted
major
risk
factors
aging.
However,
their
significance
in
or
has
not
elucidated.
Herein,
we
explain
underlying
mechanisms
protective
roles
from
a
molecular,
phenotypic
perspective.
We
provide
insights
into
broad
prospect
preventing
treating
Additionally,
highlight
gaps
for
further
studies
clinical
applications
This
review
forms
basis
on
relationship
between
RAs.