Vaccines,
Journal Year:
2015,
Volume and Issue:
3(3), P. 703 - 729
Published: Sept. 10, 2015
Indoleamine
2,
3-dioxygenase
(IDO)
is
the
first
and
rate
limiting
catabolic
enzyme
in
degradation
pathway
of
essential
amino
acid
tryptophan.
By
cleaving
aromatic
indole
ring
tryptophan,
IDO
initiates
production
a
variety
tryptophan
products
called
"kynurenines"
that
are
known
to
exert
important
immuno-regulatory
functions.
Because
must
be
supplied
diet,
regulation
catabolism
may
profound
effects
by
activating
or
inhibiting
metabolism
immune
responses.
Important
for
survival,
biosynthesis
its
activity
cells
system
can
critically
alter
their
responses
immunological
insults,
such
as
infection,
autoimmunity
cancer.
In
this
review,
we
assess
how
IDO-mediated
modulate
arrest
inflammation,
suppress
immunity
cancer
inhibit
allergy,
rejection
transplanted
tissues.
Finally,
examine
vaccines
enhance
suppression
through
upregulation
human
dendritic
cells.
Nutrients,
Journal Year:
2015,
Volume and Issue:
7(9), P. 8199 - 8226
Published: Sept. 23, 2015
Magnesium
is
the
fourth
most
abundant
mineral
in
body.
It
has
been
recognized
as
a
cofactor
for
more
than
300
enzymatic
reactions,
where
it
crucial
adenosine
triphosphate
(ATP)
metabolism.
required
DNA
and
RNA
synthesis,
reproduction,
protein
synthesis.
Moreover,
magnesium
essential
regulation
of
muscular
contraction,
blood
pressure,
insulin
metabolism,
cardiac
excitability,
vasomotor
tone,
nerve
transmission
neuromuscular
conduction.
Imbalances
status-primarily
hypomagnesemia
seen
common
hypermagnesemia-might
result
unwanted
neuromuscular,
or
nervous
disorders.
Based
on
magnesium's
many
functions
within
human
body,
plays
an
important
role
prevention
treatment
diseases.
Low
levels
have
associated
with
number
chronic
diseases,
such
Alzheimer's
disease,
resistance
type-2
diabetes
mellitus,
hypertension,
cardiovascular
disease
(e.g.,
stroke),
migraine
headaches,
attention
deficit
hyperactivity
disorder
(ADHD).
Redox Biology,
Journal Year:
2018,
Volume and Issue:
20, P. 247 - 260
Published: Oct. 20, 2018
Oxidative
stress
and
inflammation
interact
in
the
development
of
diabetic
atherosclerosis.
Intracellular
hyperglycemia
promotes
production
mitochondrial
reactive
oxygen
species
(ROS),
increased
formation
intracellular
advanced
glycation
end-products,
activation
protein
kinase
C,
polyol
pathway
flux.
ROS
directly
increase
expression
inflammatory
adhesion
factors,
oxidized-low
density
lipoprotein,
insulin
resistance.
They
activate
ubiquitin
pathway,
inhibit
AMP-protein
adiponectin,
decrease
endothelial
nitric
oxide
synthase
activity,
all
which
accelerate
Changes
composition
gut
microbiota
changes
microRNA
that
influence
regulation
target
genes
occur
diabetes
with
to
promote
This
review
highlights
consequences
sustained
acceleration
atherosclerosis
by
diabetes.
The
potential
contributions
are
discussed.
Antioxidants and Redox Signaling,
Journal Year:
2016,
Volume and Issue:
25(12), P. 657 - 684
Published: Feb. 24, 2016
Significance:
Intrarenal
oxidative
stress
plays
a
critical
role
in
the
initiation
and
progression
of
diabetic
kidney
disease
(DKD).
Enhanced
results
from
overproduction
reactive
oxygen
species
(ROS)
context
concomitant,
insufficient
antioxidant
pathways.
Renal
ROS
production
diabetes
is
predominantly
mediated
by
various
NADPH
oxidases
(NOXs),
but
defective
system
as
well
mitochondrial
dysfunction
may
also
contribute.
Recent
Advances:
Effective
agents
targeting
source
generation
hold
promise
to
rescue
damage
prevent
subsequent
DKD.
Critical
Issues
Future
Directions:
In
present
review,
we
summarize
critically
analyze
molecular
cellular
mechanisms
that
have
been
demonstrated
be
involved
NOX-induced
renal
injury
diabetes,
with
particular
focus
on
increased
glomerular
injury,
development
albuminuria,
tubulointerstitial
fibrosis,
dysfunction.
Furthermore,
novel
NOX
isoforms
are
discussed.
Antioxid.
Redox
Signal.
25,
657–684.
Oxidative Medicine and Cellular Longevity,
Journal Year:
2020,
Volume and Issue:
2020, P. 1 - 13
Published: March 9, 2020
Type
2
diabetes
mellitus
(T2DM)
is
the
most
prevalent
metabolic
disorder
characterized
by
chronic
hyperglycemia
and
an
inadequate
response
to
circulatory
insulin
peripheral
tissues
resulting
in
resistance.
Insulin
resistance
has
a
complex
pathophysiology,
it
contributed
multiple
factors
including
oxidative
stress.
Oxidative
stress
refers
imbalance
between
free
radical
production
antioxidant
system
leading
reduction
of
sensitivity
contributing
development
T2DM
via
several
molecular
mechanisms.
In
this
review,
we
present
mechanisms
which
milieu
contributes
pathophysiology
mellitus.
European Heart Journal,
Journal Year:
2015,
Volume and Issue:
36(27), P. 1718 - 1727
Published: April 17, 2015
Diabetes
mellitus-related
cardiomyopathy
(DMCMP)
was
originally
described
as
a
dilated
phenotype
with
eccentric
left
ventricular
(LV)
remodelling
and
systolic
LV
dysfunction.
Recently
however,
clinical
studies
on
DMCMP
mainly
describe
restrictive
concentric
diastolic
Both
phenotypes
are
not
successive
stages
of
but
evolve
independently
to
respectively
heart
failure
preserved
ejection
fraction
(HFPEF)
or
reduced
(HFREF).
Phenotype-specific
pathophysiological
mechanisms
were
recently
proposed
for
dysfunction
in
HFPEF
HFREF
consisting
coronary
microvascular
endothelial
cardiomyocyte
cell
death
HFREF.
A
similar
preferential
involvement
compartments
explains
development
into
distinct
restrictive/HFPEF
dilated/HFREF
phenotypes.
mellitus
(DM)-related
metabolic
derangements
such
hyperglycaemia,
lipotoxicity,
hyperinsulinaemia
favour
phenotype,
which
is
more
prevalent
obese
type
2
DM
patients.
In
contrast,
autoimmunity
predisposes
manifests
itself
autoimmune-prone
1
Finally,
rarefaction
advanced
glycation
end-products
deposition
relevant
both
Diagnosis
requires
impaired
glucose
metabolism
exclusion
coronary,
valvular,
hypertensive,
congenital
disease
viral,
toxic,
familial,
infiltrative
cardiomyopathy.
addition,
diagnosis
normal
function
dysfunction,
whereas
Treatment
limited
diuretics
lifestyle
modification,
treated
accordance
HF
guidelines.
Circulation Research,
Journal Year:
2020,
Volume and Issue:
126(11), P. 1501 - 1525
Published: May 21, 2020
Diabetes
mellitus
predisposes
affected
individuals
to
a
significant
spectrum
of
cardiovascular
complications,
one
the
most
debilitating
in
terms
prognosis
is
heart
failure.
Indeed,
increasing
global
prevalence
diabetes
and
an
aging
population
has
given
rise
epidemic
mellitus-induced
Despite
research
attention
this
phenomenon,
termed
diabetic
cardiomyopathy,
received
over
several
decades,
understanding
full
potential
contributing
mechanisms,
their
relative
contribution
failure
phenotype
specific
context
mellitus,
not
yet
been
fully
resolved.
Key
recent
preclinical
discoveries
that
comprise
current
state-of-the-art
basic
mechanisms
complex
phenotype,
is,
heart,
form
basis
review.
Abnormalities
each
cardiac
metabolism,
physiological
pathophysiological
signaling,
mitochondrial
compartment,
addition
oxidative
stress,
inflammation,
myocardial
cell
death
pathways,
neurohumoral
are
addressed.
Further,
interactions
between
these
how
they
align
functional,
morphological,
structural
impairments
characterize
considered
light
clinical
context:
from
disease
burden,
its
management
clinic,
where
knowledge
gaps
remain.
The
need
for
continued
interrogation
(both
known
those
be
identified)
essential
only
decipher
why
but
also
facilitate
improved
inroads
into
pervasive
challenge.
Nutrients,
Journal Year:
2017,
Volume and Issue:
9(12), P. 1348 - 1348
Published: Dec. 12, 2017
Increased
dietary
fiber
consumption
has
been
associated
with
many
beneficial
effects,
including
amelioration
of
obesity
and
insulin
resistance.
These
effects
may
be
due
to
the
increased
production
short
chain
fatty
acids,
propionate,
acetate
butyrate,
during
fermentation
in
colon.
Indeed,
oral
supplementation
butyrate
alone
shown
prevent
high
fat-diet
induced
This
review
focuses
on
sources
emphasis
mechanisms
metabolism
gut
its
protective
colon
cancer
peripheral
tissues
prevention
reversal