Molecular Medicine,
Год журнала:
2023,
Номер
29(1)
Опубликована: Янв. 5, 2023
Atherosclerosis
(AS),
leading
to
gradual
occlusion
of
the
arterial
lumen,
refers
accumulation
lipids
and
inflammatory
debris
in
wall.
Despite
therapeutic
advances
over
past
decades
including
intervention
or
surgery,
atherosclerosis
is
still
most
common
cause
cardiovascular
diseases
main
mechanism
death
disability
worldwide.
Vascular
smooth
muscle
cells
(VSMCs)
play
an
imperative
role
occurrence
throughout
whole
stages.
In
past,
there
was
a
lack
comprehensive
understanding
VSMCs,
but
development
identification
technology,
vivo
single-cell
sequencing
technology
lineage
tracing
with
CreERT2-loxP
system,
suggests
that
VSMCs
have
remarkable
plasticity
reevaluates
well-established
concepts
about
contribution
VSMCs.
Transcription
factors,
kind
protein
molecule
specifically
recognizes
binds
DNA
upstream
promoter
regions
distal
enhancer
elements,
key
transcription
initiation
coding
genes
are
necessary
for
RNA
polymerase
bind
gene
promoters.
this
review,
we
highlight
that,
except
environmental
VSMC
transcriptionally
regulated
through
complex
interactions
multiple
conserved
cis-regulatory
elements
factors.
addition,
series
transcription-related
regulatory
processes,
could
undergo
phenotypic
transformation,
proliferation,
migration,
calcification
apoptosis.
Finally,
enhancing
inhibiting
factors
can
regulate
atherosclerotic
lesions,
downstream
molecular
transcriptional
regulation
has
also
been
widely
studied.
Circulation,
Год журнала:
2022,
Номер
146(20), С. 1537 - 1557
Опубликована: Окт. 19, 2022
Exercise
is
an
effective
nonpharmacological
strategy
to
alleviate
diabetic
cardiomyopathy
(DCM)
through
poorly
defined
mechanisms.
FGF21
(fibroblast
growth
factor
21),
a
peptide
hormone
with
pleiotropic
benefits
on
cardiometabolic
homeostasis,
has
been
identified
as
exercise
responsive
factor.
This
study
aims
investigate
whether
signaling
mediates
the
of
DCM,
and
if
so,
elucidate
underlying
The
global
or
hepatocyte-specific
knockout
mice,
cardiomyocyte-selective
β-klotho
(the
obligatory
co-receptor
for
FGF21)
their
wild-type
littermates
were
subjected
high-fat
diet
feeding
injection
streptozotocin
induce
followed
by
6-week
intervention
assessment
cardiac
functions.
Cardiac
mitochondrial
structure
function
assessed
electron
microscopy,
enzymatic
assays,
measurements
fatty
acid
oxidation
ATP
production.
Human
induced
pluripotent
stem
cell-derived
cardiomyocytes
used
receptor
postreceptor
pathways
conferring
protective
effects
against
toxic
lipids-induced
dysfunction.
Treadmill
markedly
expression
significantly
attenuated
diabetes-induced
dysfunction
in
accompanied
reduced
damage
increased
activities
enzymes
hearts.
However,
such
cardioprotective
largely
abrogated
mice
hepatocyte-selective
ablation
FGF21,
cardiomyocyte-specific
deletion
β-klotho.
Mechanistically,
enhanced
actions
deacetylase
SIRT3
AMPK-evoked
phosphorylation
FOXO3,
thereby
reversing
hyperacetylation
functional
impairments
cluster
enzymes.
prevented
oxidative
stress
induction
AMPK/FOXO3/SIRT3
axis
human
cardiomyocytes.
Adeno-associated
virus-mediated
restoration
was
sufficient
restore
responsiveness
amelioration
DCM.
FGF21-SIRT3
DCM
preserving
integrity
represents
potential
therapeutic
target
URL:
https://www.
gov;
Unique
identifier:
NCT03240978.
Autophagy
is
a
lysosome-dependent,
self-renewal
mechanism
that
can
degrade
and
recycle
cellular
components
in
eukaryotic
cells
to
maintain
the
stability
of
intracellular
environment
ability
cope
with
unfavorable
environments.
Numerous
studies
suggest
autophagy
participates
regulating
various
functions
closely
associated
onset
progression
diseases.
Wound
healing
complex,
multistep
biological
process
involves
multiple
cell
types.
Refractory
wounds,
which
include
diabetic
skin
ulcers,
seriously
endanger
human
health.
Previous
have
confirmed
plays
an
essential
role
phases
wound
healing.
Specifically,
inflammatory
phase,
has
anti-infection
effect
it
negatively
regulates
response,
prevents
excessive
inflammation
from
causing
tissue
damage.
In
proliferative
local
hypoxia
induce
autophagy,
anti-apoptosis
anti-oxidative
stress
promotes
survival.
vascular
endothelial
angiogenesis
keratinocytes
their
differentiation,
proliferation
migration,
conducive
completion
re-epithelialisation.
remodeling
fibroblasts
affects
formation
hypertrophic
scars.
Additionally,
refractory
may
be
increased
levels
regulation
mesenchymal
stem
improve
its
application
Therefore,
understanding
relationship
between
exploring
molecular
provide
novel
strategies
for
clinical
treatment
BioMed Research International,
Год журнала:
2022,
Номер
2022, С. 1 - 12
Опубликована: Сен. 17, 2022
Oxidative
stress
is
an
imbalance
between
free
radicals
and
the
antioxidant
system
causing
overgeneration
of
(oxygen-containing
molecules)
ultimately
leading
to
oxidative
damage
in
terms
lipid
peroxidation,
protein
denaturation,
DNA
mutation.
can
activate
autophagy
alleviate
maintain
normal
physiological
activities
cells
by
degrading
damaged
organelles
or
local
cytoplasm.
When
not
eliminated
autophagy,
it
activates
apoptosis
cascade.
This
review
provides
a
brief
summary
mitochondrial-endoplasmic
reticulum
communication-mediated
autophagy.
Mitochondria
endoplasmic
being
important
are
directly
indirectly
connected
each
other
through
mitochondria-associated
membranes
jointly
regulate
The
reactive
oxygen
species
(ROS)
produced
mitochondrial
respiratory
chain
main
inducers
stress.
Damaged
mitochondria
be
effectively
cleared
process
mitophagy
mediated
PINK1/parkin
pathway,
Nix/BNIP3
pathways,
FUNDC1
avoiding
excessive
ROS
production.
However,
mechanism
communication
regulation
rarely
known.
For
this
reason,
explores
mutual
connection
mediating
Ca
Cells,
Год журнала:
2024,
Номер
13(5), С. 441 - 441
Опубликована: Март 2, 2024
Oxidative
stress
refers
to
the
imbalance
between
production
of
reactive
oxygen
species
(ROS)
and
endogenous
antioxidant
defense
system.
Its
involvement
in
cell
senescence,
apoptosis,
series
diseases
has
been
demonstrated.
Advances
carcinogenic
research
have
revealed
oxidative
as
a
pivotal
pathophysiological
pathway
tumorigenesis
be
involved
lung
cancer,
glioma,
hepatocellular
carcinoma,
leukemia,
so
on.
This
review
combs
effects
on
each
phase
fate
determination,
three
features
are
discussed.
takes
part
processes
ranging
from
tumor
death
via
pathways
like
mitochondrial
stress,
endoplasmic
reticulum
ferroptosis.
It
can
affect
by
engaging
complex
relationships
death,
cancer.
The
influence
progression
is
multi-stage
interlaced
process
that
includes
two
aspects
promotion
inhibition,
with
mitochondria
core
regulation.
A
deeper
more
comprehensive
understanding
conducive
exploring
therapies.
Redox Biology,
Год журнала:
2020,
Номер
31, С. 101488 - 101488
Опубликована: Март 9, 2020
Sex
differences
in
diseases
involving
oxidative
and
proteolytic
stress
are
common,
including
greater
ischemic
heart
disease,
Parkinson
disease
stroke
men,
Alzheimer
women.
also
observed
response
of
cells
tissues,
where
female
generally
more
resistant
to
heat
stress-induced
cell
death.
Studies
implicate
beneficial
effects
estrogen,
as
well
cell-autonomous
superior
mitochondrial
function
increased
expression
genes
relative
male
cells.
The
p53
forkhead
box
(FOX)-family
genes,
shock
proteins
(HSPs),
the
apoptosis
autophagy
pathways
appear
particularly
important
mediating
sex
response.
Antioxidants,
Год журнала:
2022,
Номер
11(9), С. 1845 - 1845
Опубликована: Сен. 19, 2022
Oxidative
stress
and
AKT
serine-threonine
kinase
(AKT)
are
responsible
for
regulating
several
cell
functions
of
cancer
cells.
Several
natural
products
modulate
both
oxidative
anticancer
effects.
However,
the
impact
product-modulating
on
lacks
systemic
understanding.
Notably,
contribution
by
downstream
effectors
is
not
yet
well
integrated.
This
review
explores
role
pathway
(AKT/AKT
effectors)
ten
functions,
including
apoptosis,
autophagy,
endoplasmic
reticulum
stress,
mitochondrial
morphogenesis,
ferroptosis,
necroptosis,
DNA
damage
response,
senescence,
migration,
cell-cycle
progression.
The
connected
to
these
through
function
mediators.
Moreover,
related
Based
this
rationale,
with
modulating
abilities
exhibit
potential
regulate
but
some
were
rarely
reported,
particularly
effectors.
sheds
light
understanding
roles
in
providing
future
directions
treatment.
Ageing Research Reviews,
Год журнала:
2022,
Номер
78, С. 101621 - 101621
Опубликована: Апрель 11, 2022
Life
expectancy
has
increased
substantially
over
the
last
150
years.
Yet
this
means
that
now
most
people
also
spend
a
greater
length
of
time
suffering
from
various
age-associated
diseases.
As
such,
delaying
age-related
functional
decline
and
extending
healthspan,
period
active
older
years
free
disease
disability,
is
an
overarching
objective
current
aging
research.
Geroprotectors,
compounds
target
pathways
causally
influence
aging,
are
increasingly
recognized
as
to
extend
healthspan
in
population.
Meanwhile,
FOXO3
emerged
geroprotective
gene
intricately
involved
healthspan.
genetic
variants
linked
human
longevity,
reduced
risks,
even
self-reported
health.
Therefore,
identification
FOXO3-activating
represents
one
direct
candidate
approaches
humans.
In
work,
we
review
activate
FOXO3,
or
lifespan
FOXO3-dependent
manner.
These
can
be
classified
pharmaceuticals,
including
PI3K/AKT
inhibitors
AMPK
activators,
antidepressants
antipsychotics,
muscle
relaxants,
HDAC
inhibitors,
nutraceuticals,
primary
metabolites
cell
growth
sustenance,
secondary
extracts,
polyphenols,
terpenoids,
other
purified
natural
compounds.
The
documented
here
provide
basis
resource
for
further
research
development,
with
ultimate
goal
promoting
healthy
longevity
