Mitochondrial Melatonin: Beneficial Effects in Protecting against Heart Failure
Life,
Journal Year:
2024,
Volume and Issue:
14(1), P. 88 - 88
Published: Jan. 5, 2024
Cardiovascular
disease
is
the
cause
of
physical
infirmity
and
thousands
deaths
annually.
Typically,
during
heart
failure,
cardiomyocyte
mitochondria
falter
in
terms
energy
production
metabolic
processing.
Additionally,
inflammation
accumulation
non-contractile
fibrous
tissue
contribute
to
cardiac
malfunction.
Melatonin,
an
endogenously
produced
molecule,
experimentally
reduces
initiation
progression
atherosclerotic
lesions,
which
are
often
basis
coronary
artery
disease.
The
current
review
critically
analyzes
published
data
related
experimental
use
melatonin
forestall
pathologies.
Collectively,
these
studies
document
melatonin’s
anti-atherosclerotic
actions
reducing
LDL
oxidation
triglyceride
levels,
lowering
endothelial
malfunction,
limiting
adhesion
molecule
formation,
preventing
macrophage
polarization
M1
pro-inflammatory
phenotype,
changing
cellular
metabolism,
scavenging
destructive
reactive
oxygen
species,
proliferation
invasion
arterial
smooth
muscle
cells
into
lesioned
area,
restricting
ingrowth
blood
vessels
from
vasa
vasorum,
solidifying
plaque
cap
reduce
chance
its
rupture.
Diabetic
hyperglycemia,
aggravates
also
inhibited
by
supplementation
animals.
potential
value
non-toxic
as
a
possible
inhibitor
pathology
humans
should
be
seriously
considered
performing
clinical
trials
using
this
multifunctional
molecule.
Language: Английский
Melatonin ameliorates PM2.5-induced airway inflammation and apoptosis by PERK/eIF2α/ATF4/CHOP in chronic obstructive pulmonary disease mice
Meng Shi,
No information about this author
Kai Liu,
No information about this author
Xin Li
No information about this author
et al.
Toxicology and Applied Pharmacology,
Journal Year:
2025,
Volume and Issue:
unknown, P. 117314 - 117314
Published: March 1, 2025
Language: Английский
Melatonin as a treatment for atherosclerosis: focus on programmed cell death, inflammation and oxidative stress
Reza Asemi,
No information about this author
Elham Omidi Najafabadi,
No information about this author
Zahra Gholami Mahmoudian
No information about this author
et al.
Journal of Cardiothoracic Surgery,
Journal Year:
2025,
Volume and Issue:
20(1)
Published: April 12, 2025
Delaying
the
development
of
atherosclerosis
(AS)
and
decreasing
cardiac
ischemia-reperfusion
damage
remain
serious
challenges
for
medical
community.
Chronic
arterial
disease,
i.e.,
AS,
is
frequently
linked
to
oxidative
stress
inflammation
as
significant
contributing
causes.
AS
risk
factors,
such
hyperlipidemia,
high
blood
pressure,
age,
hyperglycemia,
smoking,
cholesterol,
irregular
sleep
patterns,
can
exacerbate
in
carotid
artery
further
shrink
its
lumen.
Finding
new
approaches
that
support
plaque
inhibition
or
stability
an
ongoing
problem.
The
last
ten
years
have
shown
us
melatonin
(MLT)
affects
cardiovascular
system,
although
exact
mechanisms
action
are
yet
unknown.
MLT's
direct
free
radical
scavenger
activity,
indirect
antioxidant
qualities,
anti-inflammatory
capabilities
all
contribute
atheroprotective
effects
on
several
pathogenic
signaling
pathways.
Herein,
we
examine
evidence
showing
MLT
treatment
has
protective
against
AS-related
diseases.
numerous
pieces
puzzle
been
epigenetic
biogenetic
targets
prevention
therapy
atherosclerotic
processes
identified.
Language: Английский
Protective effect of vitexin against high fat-induced vascular endothelial inflammation through inhibiting trimethylamineN-oxide-mediated RNA m6A modification
Wenwen Li,
No information about this author
Zeyuan Deng,
No information about this author
Shuang Xiao
No information about this author
et al.
Food & Function,
Journal Year:
2024,
Volume and Issue:
15(13), P. 6988 - 7002
Published: Jan. 1, 2024
A
high-fat
diet
(HFD)
is
a
major
risk
factor
for
cardiovascular
disease.
Language: Английский
Melatonin and Vascular Function
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(6), P. 747 - 747
Published: June 20, 2024
The
indolamine
hormone
melatonin,
also
known
as
N-acetyl-5-methoxytrypamine,
is
frequently
associated
with
circadian
rhythm
regulation.
Light
can
suppress
melatonin
secretion,
and
photoperiod
regulates
levels
by
promoting
its
production
secretion
at
night
in
response
to
darkness.
This
becoming
more
understood
for
functions
an
immune-modulatory,
anti-inflammatory,
antioxidant
hormone.
Melatonin
may
have
a
major
effect
on
several
diabetes-related
disturbances,
such
hormonal
imbalances,
oxidative
stress,
sleep
mood
disorders,
according
recent
research.
has
raised
interest
investigating
the
possible
therapeutic
advantages
of
treatment
diabetic
complications.
In
addition,
studies
described
that
been
linked
development
diabetes,
cancer,
Alzheimer’s
disease,
immune
system
heart
diseases.
this
review,
we
will
highlight
some
regarding
vascular
biology.
Language: Английский
Melatonin stabilizes atherosclerotic plaques: an association that should be clinically exploited
Frontiers in Medicine,
Journal Year:
2024,
Volume and Issue:
11
Published: Dec. 11, 2024
Atherosclerosis
is
the
underlying
factor
in
premature
death
of
millions
humans
annually.
The
cause
often
a
result
rupture
an
atherosclerotic
plaque
followed
by
discharge
associated
molecular
debris
into
vessel
lumen
which
occludes
artery
leading
to
ischemia
downstream
tissue
and
morbidity
or
mortality
individual.
This
most
serious
when
it
occurs
heart
(heart
attack)
brain
(stroke).
Atherosclerotic
plaques
are
classified
as
either
soft,
rupture-prone,
hard,
resistant.
Melatonin,
production
diminishes
with
age,
has
major
actions
converting
soft
hard
plaques.
Experimentally,
melatonin
reduces
ingrowth
capillaries
from
tunica
media
relieving
pressure
on
plaque,
reducing
intraplaque
hemorrhage
limiting
size
necrotic
core.
Moreover,
promotes
formation
collagen
invading
vascular
smooth
muscle
cells
strengthen
crown
making
resistant
rupture.
Melatonin
also
powerful
antioxidant
anti-inflammatory
agent
such
that
oxidative
damage
tissues
limits
inflammation
both
contribute
cap
weakness.
Additional
benefits
relative
atherosclerosis
inhibition
adhesion
molecules
endothelial
cell
surface,
invasion
monocytes
arterial
intima,
conversion
M2
macrophages
pro-inflammatory
M1
macrophages.
Given
high
physiological
financial
cost
cardiac
neural
ischemic
events,
this
information
should
be
given
priority
clinical
setting.
Language: Английский
The Identification of Key Genes and Biological Pathways in Cardiac Arrest by Integrated Bioinformatics and Next Generation Sequencing Data Analysis
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: Aug. 19, 2024
Abstract
Cardiac
arrest
(CA)
is
a
common
cause
of
death
world
wide.
The
disease
has
lacks
effective
treatment.
Efforts
have
been
made
to
elucidate
the
molecular
pathogenesis
CA,
but
mechanisms
remain
elusive.
To
identify
key
genes
and
pathways
in
next
generation
sequencing
(NGS)
GSE200117
dataset
was
downloaded
from
Gene
Expression
Omnibus
(GEO)
database.
DESeq2
tool
used
recognize
differentially
expressed
(DEGs).
ontology
(GO)
REACTOME
pathway
enrichment
analyses
were
performed
analyze
DEGs
associated
signal
g:Profiler
IID
database
construct
protein-protein
interaction
(PPI)
network,
modules
analysis
using
Cytoscape.
A
miRNA-hub
gene
regulatory
network
TF-hub
then
constructed
screen
miRNAs,
TFs
hub
by
miRNet
NetworkAnalyst
Cityscape
software.
Receiver
operating
characteristic
curve
(ROC)
verified
genes.
In
total,
844
identified,
comprising
414
up
regulated
430
down
GO
indicated
that
for
CA
mainly
enriched
organonitrogen
compound
metabolic
process,
response
stimulus,
translation
immune
system.
Ten
(up-regulated:
HSPA8,
HOXA1,
INCA1
TP53;
down-regulated:
HSPB1,
LMNA,
SNCA,
ADAMTSL4
PDLIM7)
screened.
We
also
predicted
miRNAs
(hsa-mir-1914-5p
hsa-mir-598-3p)
(JUN
PRRX2)
targeting
This
study
uses
series
bioinformatics
technologies
obtain
hug
genes,
TFs,
related
CA.
These
results
provide
us
with
new
ideas
finding
biomarkers
treatment
methods
Language: Английский