Cells,
Journal Year:
2019,
Volume and Issue:
8(11), P. 1436 - 1436
Published: Nov. 14, 2019
Physical
exercise
promotes
cardiorespiratory
fitness,
and
is
considered
the
mainstream
of
non-pharmacological
therapies
along
with
lifestyle
modification
for
various
chronic
diseases,
in
particular
cardiovascular
diseases.
may
positively
affect
risk
factors
including
body
weight,
blood
pressure,
insulin
sensitivity,
lipid
glucose
metabolism,
heart
function,
endothelial
fat
composition.
With
ever-rising
prevalence
obesity
other
types
metabolic
as
well
sedentary
lifestyle,
regular
moderate
intensity
has
been
indicated
to
benefit
health
reduce
overall
disease
mortality.
Exercise
offers
a
wide
cadre
favorable
responses
system
such
improved
dynamics
system,
reduced
coronary
diseases
cardiomyopathies,
enhanced
cardiac
reserve
capacity,
autonomic
regulation.
Ample
clinical
experimental
evidence
an
emerging
role
autophagy,
conservative
catabolism
process
degrade
recycle
cellular
organelles
nutrients,
training-offered
benefits.
Regular
physical
unique
form
physiological
stress
capable
triggering
adaptation
while
autophagy
selective
seems
be
permissive
adaptation.
Here
this
mini-review,
we
will
summarize
mitochondrial
namely
mitophagy
versus
on
function.
The EMBO Journal,
Journal Year:
2021,
Volume and Issue:
40(19)
Published: Aug. 30, 2021
Review30
August
2021Open
Access
Autophagy
in
major
human
diseases
Daniel
J
Klionsky
orcid.org/0000-0002-7828-8118
Life
Sciences
Institute,
University
of
Michigan,
Ann
Arbor,
MI,
USA
Search
for
more
papers
by
this
author
Giulia
Petroni
Department
Radiation
Oncology,
Weill
Cornell
Medical
College,
New
York,
NY,
Ravi
K
Amaravadi
Medicine,
Pennsylvania,
Philadelphia,
PA,
Abramson
Cancer
Center,
Eric
H
Baehrecke
Molecular,
Cell
and
Biology,
Massachusetts
School,
Worcester,
MA,
Andrea
Ballabio
orcid.org/0000-0003-1381-4604
Telethon
Institute
Genetics
Pozzuoli,
Italy
Translational
Sciences,
Section
Pediatrics,
Federico
II
University,
Naples,
Molecular
Human
Genetics,
Baylor
College
Jan
Dan
Duncan
Neurological
Research
Texas
Children
Hospital,
Houston,
TX,
Patricia
Boya
orcid.org/0000-0003-3045-951X
Margarita
Salas
Center
Biological
Research,
Spanish
National
Council,
Madrid,
Spain
José
Manuel
Bravo-San
Pedro
Faculty
Physiology,
Complutense
Networked
Biomedical
Neurodegenerative
Diseases
(CIBERNED),
Ken
Cadwell
Kimmel
Biology
Medicine
at
the
Skirball
York
Grossman
School
Microbiology,
Division
Gastroenterology
Hepatology,
Langone
Health,
Francesco
Cecconi
orcid.org/0000-0002-5614-4359
Stress
Survival
Unit,
Autophagy,
Recycling
Disease
(CARD),
Danish
Society
Copenhagen,
Denmark
Pediatric
Onco-Hematology
Gene
Therapy,
IRCCS
Bambino
Gesù
Children's
Rome,
Rome
'Tor
Vergata',
Augustine
M
Choi
Pulmonary
Critical
Care
Joan
Sanford
I.
York-Presbyterian
Mary
E
Nephrology
Hypertension,
Charleen
T
Chu
orcid.org/0000-0002-5052-8271
Pathology,
Pittsburgh
Pittsburgh,
Patrice
Codogno
orcid.org/0000-0002-5492-3180
Institut
Necker-Enfants
Malades,
INSERM
U1151-CNRS
UMR
8253,
Paris,
France
Université
de
Maria
Isabel
Colombo
Laboratorio
Mecanismos
Moleculares
Implicados
en
el
Tráfico
Vesicular
y
la
Autofagia-Instituto
Histología
Embriología
(IHEM)-Universidad
Nacional
Cuyo,
CONICET-
Facultad
Ciencias
Médicas,
Mendoza,
Argentina
Ana
Cuervo
orcid.org/0000-0002-0771-700X
Developmental
Albert
Einstein
Bronx,
Aging
Studies,
Vojo
Deretic
Inflammation
Metabolism
(AIM,
Excellence,
Mexico
Health
Albuquerque,
NM,
Ivan
Dikic
orcid.org/0000-0001-8156-9511
Biochemistry
II,
Goethe
Frankfurt,
Frankfurt
am
Main,
Germany
Buchmann
Zvulun
Elazar
Biomolecular
The
Weizmann
Science,
Rehovot,
Israel
Eeva-Liisa
Eskelinen
Biomedicine,
Turku,
Finland
Gian
Fimia
orcid.org/0000-0003-4438-3325
Sapienza
Epidemiology,
Preclinical
Advanced
Diagnostics,
Infectious
'L.
Spallanzani'
IRCCS,
David
A
Gewirtz
orcid.org/0000-0003-0437-4934
Pharmacology
Toxicology,
Virginia
Commonwealth
Richmond,
VA,
Douglas
R
Green
Immunology,
St.
Jude
Memphis,
TN,
Malene
Hansen
Burnham
Prebys
Discovery
Program
Development,
Aging,
Regeneration,
La
Jolla,
CA,
Marja
Jäättelä
orcid.org/0000-0001-5950-7111
Death
Metabolism,
&
Disease,
Cellular
Terje
Johansen
orcid.org/0000-0003-1451-9578
Group,
Tromsø—The
Arctic
Norway,
Tromsø,
Norway
Gábor
Juhász
Szeged,
Hungary
Anatomy,
Eötvös
Loránd
Budapest,
Vassiliki
Karantza
Merck
Co.,
Inc.,
Kenilworth,
NJ,
Claudine
Kraft
orcid.org/0000-0002-3324-4701
ZBMZ,
Freiburg,
CIBSS
-
Centre
Integrative
Signalling
Guido
Kroemer
orcid.org/0000-0002-9334-4405
Recherche
des
Cordeliers,
Equipe
Labellisée
par
Ligue
Contre
le
Cancer,
Sorbonne
Université,
Inserm
U1138,
Universitaire
France,
Metabolomics
Platforms,
Gustave
Roussy,
Villejuif,
Pôle
Biologie,
Hôpital
Européen
Georges
Pompidou,
AP-HP,
Suzhou
Systems
Chinese
Academy
Suzhou,
China
Karolinska
Women's
Stockholm,
Sweden
Nicholas
Ktistakis
Programme,
Babraham
Cambridge,
UK
Sharad
Kumar
orcid.org/0000-0001-7126-9814
South
Australia,
Adelaide,
SA,
Australia
Carlos
Lopez-Otin
orcid.org/0000-0001-6964-1904
Departamento
Bioquímica
Biología
Medicina,
Instituto
Universitario
Oncología
del
Principado
Asturias
(IUOPA),
Universidad
Oviedo,
Centro
Investigación
Biomédica
Red
Cáncer
(CIBERONC),
Kay
F
Macleod
Ben
May
Gordon
W-338,
Chicago,
IL,
Frank
Madeo
Biosciences,
NAWI
Graz,
Austria
BioTechMed-Graz,
Field
Excellence
BioHealth
–
Jennifer
Martinez
Immunity,
Laboratory,
Environmental
NIH,
Triangle
Park,
NC,
Alicia
Meléndez
Department,
Queens
City
Flushing,
Graduate
PhD
Programs
Noboru
Mizushima
orcid.org/0000-0002-6258-6444
Tokyo,
Japan
Christian
Münz
orcid.org/0000-0001-6419-1940
Viral
Immunobiology,
Experimental
Zurich,
Switzerland
Josef
Penninger
Biotechnology
Austrian
(IMBA),
Vienna
BioCenter
(VBC),
Vienna,
British
Columbia,
Vancouver,
BC,
Canada
Rushika
Perera
orcid.org/0000-0003-2435-2273
California,
San
Francisco,
Helen
Diller
Family
Comprehensive
Mauro
Piacentini
orcid.org/0000-0003-2919-1296
"Tor
Vergata",
Laboratory
Cytology
Russian
Saint
Petersburg,
Russia
Fulvio
Reggiori
orcid.org/0000-0003-2652-2686
Cells
Systems,
Section,
Groningen,
Netherlands
C
Rubinsztein
Cambridge
Dementia
Kevin
Ryan
Beatson
Glasgow,
Junichi
Sadoshima
Cardiovascular
Rutgers
Jersey
Newark,
Laura
Santambrogio
Sandra
Edward
Meyer
Caryl
Englander
Precision
Luca
Scorrano
orcid.org/0000-0002-8515-8928
Istituto
Veneto
di
Medicina
Molecolare,
Padova,
Hans-Uwe
Simon
Pharmacology,
Bern,
Clinical
Immunology
Allergology,
Sechenov
Moscow,
Fundamental
Kazan
Federal
Kazan,
Anna
Katharina
Kennedy
Rheumatology,
NDORMS,
Oxford,
Anne
Simonsen
orcid.org/0000-0003-4711-7057
Basic
Oslo,
Reprogramming,
Oslo
Hospital
Montebello,
Alexandra
Stolz
orcid.org/0000-0002-3340-439X
Nektarios
Tavernarakis
orcid.org/0000-0002-5253-1466
Biotechnology,
Foundation
Technology-Hellas,
Heraklion,
Crete,
Greece
Sharon
Tooze
orcid.org/0000-0002-2182-3116
Francis
Crick
London,
Tamotsu
Yoshimori
orcid.org/0000-0001-9787-3788
Osaka
Suita,
Intracellular
Membrane
Dynamics,
Frontier
Integrated
Science
Division,
Open
Transdisciplinary
Initiatives
(OTRI),
Junying
Yuan
Interdisciplinary
on
Chemistry,
Shanghai
Organic
Shanghai,
Harvard
Boston,
Zhenyu
Yue
Neurology,
Friedman
Brain
Icahn
Mount
Sinai,
Qing
Zhong
orcid.org/0000-0001-6979-955X
Key
Differentiation
Apoptosis
Ministry
Education,
Pathophysiology,
Jiao
Tong
(SJTU-SM),
Lorenzo
Galluzzi
Corresponding
Author
[email
protected]
orcid.org/0000-0003-2257-8500
Dermatology,
Yale
Haven,
CT,
Pietrocola
orcid.org/0000-0002-2930-234X
Biosciences
Nutrition,
Huddinge,
mor
Biomedicine & Pharmacotherapy,
Journal Year:
2021,
Volume and Issue:
137, P. 111315 - 111315
Published: Feb. 7, 2021
Currently,
obesity
has
become
a
global
health
issue
and
is
referred
to
as
an
epidemic.
Dysfunctional
obese
adipose
tissue
plays
pivotal
role
in
the
development
of
insulin
resistance.
However,
mechanism
how
dysfunctional
obese-adipose
develops
insulin-resistant
circumstances
remains
poorly
understood.
Therefore,
this
review
attempts
highlight
potential
mechanisms
behind
obesity-associated
Multiple
risk
factors
are
directly
or
indirectly
associated
with
increased
obesity;
among
them,
environmental
factors,
genetics,
aging,
gut
microbiota,
diets
prominent.
Once
individual
becomes
obese,
adipocytes
increase
their
size;
therefore,
tissues
larger
dysfunctional,
recruit
macrophages,
then
these
polarize
pro-inflammatory
states.
Enlarged
release
excess
free
fatty
acids
(FFAs),
reactive
oxygen
species
(ROS),
cytokines.
Excess
systemic
FFAs
dietary
lipids
enter
inside
cells
non-adipose
organs
such
liver,
muscle,
pancreas,
deposited
ectopic
fat,
generating
lipotoxicity.
Toxic
dysregulate
cellular
organelles,
e.g.,
mitochondria,
endoplasmic
reticulum,
lysosomes.
Dysregulated
organelles
ROS
pro-inflammation,
resulting
inflammation.
Long
term
low-grade
inflammation
prevents
from
its
action
signaling
pathway,
disrupts
glucose
homeostasis,
results
dysregulation.
Overall,
long-term
overnutrition
develop
into
resistance
chronic
through
lipotoxicity,
creating
clinical
conditions.
This
also
shows
that
liver
most
sensitive
organ
undergoing
impairment
faster
than
other
organs,
thus,
hepatic
primary
event
leads
subsequent
peripheral
Frontiers in Endocrinology,
Journal Year:
2023,
Volume and Issue:
14
Published: April 21, 2023
The
prevalence
of
obesity
and
diabetes
mellitus
(DM)
has
been
consistently
increasing
worldwide.
Sharing
powerful
genetic
environmental
features
in
their
pathogenesis,
amplifies
the
impact
susceptibility
factors
on
DM.
ectopic
expansion
adipose
tissue
excessive
accumulation
certain
nutrients
metabolites
sabotage
metabolic
balance
via
insulin
resistance,
dysfunctional
autophagy,
microbiome-gut-brain
axis,
further
exacerbating
dysregulation
immunometabolism
through
low-grade
systemic
inflammation,
leading
to
an
accelerated
loss
functional
β-cells
gradual
elevation
blood
glucose.
Given
these
intricate
connections,
most
available
treatments
type
2
DM
(T2DM)
have
a
mutual
effect
each
other.
For
example,
anti-obesity
drugs
can
be
anti-diabetic
some
extent,
medicines,
contrast,
shown
increase
body
weight,
such
as
insulin.
Meanwhile,
surgical
procedures,
especially
bariatric
surgery,
are
more
effective
for
both
T2DM.
Besides
guaranteeing
availability
accessibility
all
diagnostic
therapeutic
tools,
clinical
experimental
investigations
pathogenesis
two
diseases
warranted
improve
efficacy
safety
newly
developed
treatments.
Physiological Reviews,
Journal Year:
2021,
Volume and Issue:
101(4), P. 1745 - 1807
Published: May 5, 2021
The
prevalence
of
heart
failure
is
on
the
rise
and
imposes
a
major
health
threat,
in
part,
due
to
rapidly
increased
overweight
obesity.
To
this
point,
epidemiological,
clinical,
experimental
evidence
supports
existence
unique
disease
entity
termed
"obesity
cardiomyopathy,"
which
develops
independent
hypertension,
coronary
disease,
other
diseases.
Our
contemporary
review
evaluates
for
pathological
condition,
examines
putative
responsible
mechanisms,
discusses
therapeutic
options
disorder.
Clinical
findings
have
consolidated
presence
left
ventricular
dysfunction
Experimental
investigations
uncovered
pathophysiological
changes
myocardial
structure
function
genetically
predisposed
diet-induced
Indeed,
consolidates
wide
array
cellular
molecular
mechanisms
underlying
etiology
obesity
cardiomyopathy
including
adipose
tissue
dysfunction,
systemic
inflammation,
metabolic
disturbances
(insulin
resistance,
abnormal
glucose
transport,
spillover
free
fatty
acids,
lipotoxicity,
amino
acid
derangement),
altered
intracellular
especially
mitochondrial
Ca2+
homeostasis,
oxidative
stress,
autophagy/mitophagy
defect,
fibrosis,
dampened
flow
reserve,
microvascular
(microangiopathy),
endothelial
impairment.
Given
important
role
risk
failure,
that
with
preserved
systolic
recent
rises
COVID-19-associated
cardiovascular
mortality,
should
provide
compelling
cardiomyopathy,
various
comorbid
conditions,
offer
new
insights
into
potential
approaches
(pharmacological
lifestyle
modification)
clinical
management
cardiomyopathy.