Journal of Advanced Research,
Journal Year:
2024,
Volume and Issue:
65, P. 297 - 327
Published: May 14, 2024
Autophagy
is
an
evolutionarily
conserved
turnover
process
for
intracellular
substances
in
eukaryotes,
relying
on
lysosomal
(in
animals)
or
vacuolar
yeast
and
plants)
mechanisms.
In
the
past
two
decades,
emerging
evidence
suggests
that,
under
specific
conditions,
autophagy
can
target
particular
macromolecules
organelles
degradation,
a
termed
selective
autophagy.
Recently,
accumulating
studies
have
demonstrated
that
abnormality
of
closely
associated
with
occurrence
progression
many
human
diseases,
including
neurodegenerative
cancers,
metabolic
cardiovascular
diseases.
This
review
aims
at
systematically
comprehensively
introducing
its
role
various
while
unravelling
molecular
mechanisms
By
providing
theoretical
basis
development
related
small-molecule
drugs
as
well
treating
this
seeks
to
contribute
understanding
therapeutic
potential.
review,
we
introduce
dissect
major
categories
been
discovered.
We
also
focus
recent
advances
underlying
both
classical
non-classical
Moreover,
current
situation
targeting
different
types
further
summarized,
valuable
insights
into
discovery
more
candidate
future.
On
other
hand,
reveal
clinically
relevant
implementations
are
potentially
autophagy,
such
predictive
approaches
treatments
tailored
individual
patients.
Frontiers in Immunology,
Journal Year:
2025,
Volume and Issue:
16
Published: Feb. 7, 2025
Metabolic
syndrome
(Mets)
is
an
important
contributor
to
morbidity
and
mortality
in
cardiovascular,
liver,
neurological,
reproductive
diseases.
Short-chain
fatty
acid
(SCFA),
organismal
energy
donor,
has
recently
been
demonstrated
increasing
number
of
studies
be
molecule
ameliorating
immuno-inflammation,
causative
factor
Mets,
improve
lipid
distribution,
blood
glucose,
body
weight
levels
animal
models
Mets.
This
study
reviews
recent
research
advances
on
SCFA
Mets
from
immune-inflammatory
perspective,
including
complications
dominated
by
chronic
inflammation,
as
well
the
fact
that
these
findings
also
contribute
understanding
specific
mechanisms
which
gut
flora
metabolites
metabolic
processes
humans.
review
proposes
emerging
role
for
inflammatory
followed
identification
major
ambiguities
further
understand
anti-inflammatory
potential
this
substance
In
addition,
novel
strategies
modulate
treatment
may
help
mitigate
prognosis
its
complications.
Cell Death and Disease,
Journal Year:
2021,
Volume and Issue:
12(6)
Published: May 28, 2021
Maintaining
proper
mitochondrial
respiratory
function
is
crucial
for
alleviating
cardiac
metabolic
disorders
during
obesity,
and
mitophagy
critically
involved
in
this
process.
Long
non-coding
RNA
H19
(H19)
regulation,
but
its
roles
disorders,
function,
obesity
are
largely
unknown.
In
study,
palmitic
acid
(PA)-treated
H9c2
cell
Lep-/-
mice
were
used
to
investigate
vitro
vivo,
respectively.
The
effects
of
on
investigated.
Moreover,
the
regulatory
mechanisms
PA,
H19,
mitophagy,
examined.
models
tested
displayed
a
reduction
expression,
number
volume,
while
expression
mitophagy-
Pink1/Parkin
signaling-related
proteins
was
upregulated,
as
indicated
using
quantitative
real-time
PCR,
Seahorse
stress
test
analyzer,
transmission
electron
microscopy,
fluorescence
indicators
western
blotting.
Forced
helped
recoveries
capacity
inhibited
levels
proteins.
Pink1
knockdown
also
attenuated
PA-induced
increased
capacity.
Mechanistically,
pull-down,
mass
spectrometry,
RNA-binding
protein
immunoprecipitation
assays
showed
that
could
hinder
binding
eukaryotic
translation
initiation
factor
4A,
isoform
2
(eIF4A2)
with
mRNA,
thus
inhibiting
attenuation
mitophagy.
PA
significantly
methylation
promoter
region
by
upregulation
Dnmt3b
methylase
levels,
thereby
transcription.
Collectively,
these
findings
suggest
DNA
methylation-mediated
downregulation
plays
role
cardiomyocyte
or
cells
induces
dysfunction
promoting
inhibits
excessive
limiting
mRNA
translation,
defect
occurs
obesity.
Oxidative Medicine and Cellular Longevity,
Journal Year:
2021,
Volume and Issue:
2021(1)
Published: Jan. 1, 2021
Abnormal
function
of
suborganelles
such
as
mitochondria
and
endoplasmic
reticulum
often
leads
to
abnormal
cardiomyocytes
or
vascular
endothelial
cells
cardiovascular
disease
(CVD).
Mitochondria‐associated
membrane
(MAM)
is
involved
in
several
important
cellular
functions.
Increasing
evidence
shows
that
MAM
the
pathogenesis
CVD.
mediates
multiple
processes,
including
calcium
homeostasis
regulation,
lipid
metabolism,
unfolded
protein
response,
ROS,
mitochondrial
dynamics,
autophagy,
apoptosis,
inflammation,
which
are
key
risk
factors
for
In
this
review,
we
discuss
structure
MAM‐associated
proteins,
their
role
CVD
progression,
potential
use
therapeutic
targets
treatment.
Frontiers in Cell and Developmental Biology,
Journal Year:
2021,
Volume and Issue:
9
Published: Sept. 27, 2021
Cardiovascular
disease
is
the
leading
complication
of
diabetes
mellitus
(DM),
and
diabetic
cardiomyopathy
(DCM)
a
major
cause
mortality
in
patients.
Multiple
pathophysiologic
mechanisms,
including
myocardial
insulin
resistance,
oxidative
stress
inflammation,
are
involved
development
DCM.
Recent
studies
have
shown
that
mitochondrial
dysfunction
makes
substantial
contribution
to
Mitophagy
type
autophagy
takes
place
dysfunctional
mitochondria,
it
plays
key
role
quality
control.
Although
precise
molecular
mechanisms
mitophagy
DCM
yet
be
fully
clarified,
recent
findings
imply
improves
cardiac
function
heart.
However,
excessive
may
exacerbate
damage
patients
with
In
this
review,
we
aim
provide
comprehensive
overview
control
dual
roles
We
also
propose
balance
between
biogenesis
essential
for
maintenance
cellular
metabolism
Medicinal Research Reviews,
Journal Year:
2022,
Volume and Issue:
43(1), P. 5 - 30
Published: Aug. 17, 2022
Abstract
The
endoplasmic
reticulum
(ER)
governs
the
proper
folding
of
polypeptides
and
proteins
through
various
chaperones
enzymes
residing
within
ER
organelle.
Perturbation
in
process
ensues
when
overwhelmed
protein
exceeds
handling
capacity,
leading
to
accumulation
misfolded/unfolded
lumen—a
state
being
referred
as
stress.
In
turn,
stress
induces
a
gamut
signaling
cascades,
termed
“unfolded
response”
(UPR)
that
reinstates
homeostasis
panel
gene
expression
modulation.
This
type
UPR
is
usually
deemed
“adaptive
UPR.”
However,
persistent
or
unresolved
hyperactivates
response,
which
ultimately,
triggers
cell
death
inflammatory
pathways,
“maladaptive/terminal
A
plethora
evidence
indicates
crosstalks
between
(maladaptive
UPR)
inflammation
precipitate
obesity
pathogenesis.
this
regard,
acquisition
mechanisms
linking
might
unveil
potential
remedies
tackle
pathological
condition.
Herein,
we
aim
elucidate
key
stress‐induced
context
summarize
therapeutic
strategies
management
maneuvering
stress‐associated
inflammation.
Frontiers in Cardiovascular Medicine,
Journal Year:
2022,
Volume and Issue:
9
Published: June 17, 2022
Mitochondria
play
a
key
role
in
cellular
metabolism.
Mitochondrial
dynamics
(fusion
and
fission)
mitophagy,
are
critical
to
mitochondrial
function.
Fusion
allows
organelles
share
metabolites,
proteins,
DNA,
promoting
complementarity
between
damaged
mitochondria.
Fission
increases
the
number
of
mitochondria
ensure
that
they
passed
on
their
offspring
during
mitosis.
Mitophagy
is
process
selective
removal
excess
or
helps
improve
energy
Cardiometabolic
disease
characterized
by
dysfunction,
high
production
reactive
oxygen
species,
increased
inflammatory
response,
low
levels
ATP.
closely
related
mitophagy.
This
paper
reviewed
mechanisms
mitophagy
(focus
MFN1,
MFN2,
OPA1,
DRP1,
PINK1
proteins)
roles
diabetic
cardiomyopathy,
myocardial
infarction,
cardiac
hypertrophy,
heart
failure,
atherosclerosis,
obesity.
