Molecules and Cells,
Journal Year:
2022,
Volume and Issue:
45(11), P. 763 - 770
Published: Nov. 1, 2022
Caenorhabditis
elegans
has
been
used
as
a
major
model
organism
to
identify
genetic
factors
that
regulate
organismal
aging
and
longevity.Insulin/insulin-like
growth
factor
1
(IGF-1)
signaling
(IIS)
regulates
in
many
species,
ranging
from
nematodes
humans.C.
is
nonpathogenic
nematode
model,
which
extensively
utilized
molecular
cellular
components
function
longevity.Here,
we
review
the
recent
progress
role
of
IIS
longevity,
involves
direct
regulation
protein
RNA
homeostasis,
stress
resistance,
metabolism
activities
endocrine
system.We
also
discuss
recently
identified
interact
with
canonical
health
span
C.
elegans.We
expect
this
provide
valuable
insights
into
understanding
animal
aging,
could
eventually
help
develop
anti-aging
drugs
for
humans.
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
Aging
is
a
complex
biological
process
characterized
by
hallmark
features
accumulating
over
the
life
course,
shaping
individual's
aging
trajectory
and
subsequent
disease
risks.
There
substantial
individual
variability
in
between
men
women.
In
general,
women
live
longer
than
men,
consistent
with
lower
ages
as
assessed
molecular
biomarkers,
but
there
paradox.
Women
are
frailer
have
worse
health
at
end
of
life,
while
still
perform
better
physical
function
examinations.
Moreover,
many
age-related
diseases
show
sex-specific
patterns.
this
review,
we
aim
to
summarize
current
knowledge
on
sexual
dimorphism
human
studies,
support
from
animal
research,
illnesses.
We
also
attempt
place
it
context
theories
aging,
well
discuss
explanations
for
sex
differences,
example,
sex-chromosome
linked
mechanisms
hormonally
driven
differences.
International Journal of Molecular Sciences,
Journal Year:
2021,
Volume and Issue:
22(23), P. 13173 - 13173
Published: Dec. 6, 2021
Cellular
senescence
entails
a
state
of
an
essentially
irreversible
proliferative
arrest
in
which
cells
remain
metabolically
active
and
secrete
range
pro-inflammatory
proteolytic
factors
as
part
the
senescence-associated
secretory
phenotype.
There
are
different
types
senescent
cells,
can
be
induced
response
to
many
DNA
damage
signals.
Senescent
accumulate
tissues
organs
where
they
have
distinct
physiological
pathological
functions.
Despite
this
diversity,
all
must
able
survive
nondividing
while
protecting
themselves
from
positive
feedback
loops
linked
constant
activation
response.
This
capacity
requires
changes
core
cellular
programs.
Understanding
how
cell
undergo
extensive
their
transcriptional
programs,
metabolism,
heterochromatin
patterns,
structures
induce
common
is
crucial
preventing
cancer
development/progression
improving
health
during
aging.
In
review,
we
discuss
continuously
evolve
after
initial
highlight
unifying
features
that
define
state.
Journal of Clinical Investigation,
Journal Year:
2022,
Volume and Issue:
132(10)
Published: May 15, 2022
Alzheimer's
disease
and
related
dementias
(ADRD)
are
among
the
top
contributors
to
disability
mortality
in
later
life.
As
with
many
chronic
conditions,
aging
is
single
most
influential
factor
development
of
ADRD.
Even
older
adults
who
remain
free
dementia
throughout
their
lives,
cognitive
decline
neurodegenerative
changes
appreciable
advancing
age,
suggesting
shared
pathophysiological
mechanisms.
In
this
Review,
we
provide
an
overview
cognition,
brain
morphology,
neuropathological
protein
accumulation
across
lifespan
humans,
complementary
mechanistic
evidence
from
animal
models.
Next,
highlight
selected
processes
that
differentially
regulated
disease,
including
aberrant
autophagy,
mitochondrial
dysfunction,
cellular
senescence,
epigenetic
changes,
cerebrovascular
inflammation,
lipid
dysregulation.
We
summarize
research
clinical
translational
studies
link
biological
underlying
ADRD
pathogenesis.
Targeting
fundamental
may
represent
a
yet
relatively
unexplored
avenue
attenuate
both
age-related
Collaboration
fields
geroscience
neuroscience,
coupled
new
models
more
closely
align
human
processes,
necessary
advance
novel
therapeutic
discovery
realm.
Nature Communications,
Journal Year:
2021,
Volume and Issue:
12(1)
Published: Jan. 28, 2021
Abstract
Low
muscle
strength
is
an
important
heritable
indicator
of
poor
health
linked
to
morbidity
and
mortality
in
older
people.
In
a
genome-wide
association
study
meta-analysis
256,523
Europeans
aged
60
years
over
from
22
cohorts
we
identify
15
loci
associated
with
weakness
(European
Working
Group
on
Sarcopenia
Older
People
definition:
n
=
48,596
cases,
18.9%
total),
including
12
not
implicated
previous
analyses
continuous
measures
grip
strength.
Loci
include
genes
reportedly
involved
autoimmune
disease
(
HLA-DQA1
p
4
×
10
−17
),
arthritis
GDF5
−13
cell
cycle
control
cancer
protection,
regulation
transcription,
others
the
development
maintenance
musculoskeletal
system.
Using
Mendelian
randomization
report
possible
overlapping
causal
pathways,
diabetes
susceptibility,
haematological
parameters,
immune
We
conclude
that
adults
has
distinct
mechanisms
strength,
several
pathways
considered
be
hallmarks
ageing.
The Journals of Gerontology Series A,
Journal Year:
2021,
Volume and Issue:
77(1), P. 94 - 100
Published: Aug. 3, 2021
Abstract
Background
The
World
Health
Organization
has
proposed
a
model
of
healthy
aging
built
around
the
concept
functional
ability,
comprising
an
individual’s
intrinsic
capacity,
physical
and
social
environment
they
occupy,
interactions
between
two.
However,
these
constructs
have
been
poorly
defined.
We
examined
structure
capacity
in
representative
sample
Chinese
population
aged
60
years
older
assessed
its
value
predicting
declining
performance
instrumental
activities
daily
living
(IADLs)
(ADLs)
using
similar
methods
to
construct
validation
previously
undertaken
English
cohort.
Methods
Deidentified
data
were
accessed
on
7
643
participants
China
Retirement
Longitudinal
Study
2011
2013
waves.
Incrementally
related
structural
equation
modeling
was
applied,
including
exploratory
confirmatory
factor
analysis,
path
analysis.
Multiple
linear
regression
tested
validity,
simple
serial
mediation
models
predictive
validity.
Results
Factor
loadings
for
showed
clear
capacity:
1
general
with
5
subfactors—locomotor,
cognitive,
psychological
sensory
capacities,
vitality
(reflecting
underlying
physiologic
changes).
Intrinsic
predicted
both
IADLs
(standardized
coefficient
(SE)
−0.324
(0.02),
p
<
.001)
ADLs
(−0.227
(0.03),
.001),
after
accounting
age,
sex,
education,
wealth,
number
chronic
diseases.
Each
characteristic
associated
providing
strong
Conclusions
Assessment
provides
valuable
information
subsequent
functioning
beyond
that
afforded
by
other
personal
factors,
multimorbidity.