Evidence map›Paper›PMID 27174950›Full record

ReviewCirculation research2016

Aging and Autophagy in the Heart.

Akihiro Shirakabe, Yoshiyuki Ikeda, Sebastiano Sciarretta, Daniela K Zablocki, Junichi Sadoshima

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 256 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
256citing papers in PubMed, 2 pooled it
28.1field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

256 citing papers in PubMed, 2 syntheses or guidelines pooled it, 433 citations in OpenAlex.

  1. Pooled it
  2. Consequences of Aging on Bone.Aging and disease · 2023
    Pooled it
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  9. Reference ranges for myocardial native T1, T2, and extracellular volume at 5.0T cardiac magnetic resonance imaging in healthy adults.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2026
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196 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Akihiro ShirakabeFrom the Department of Cell Biology and Molecular Medicine, Rutgers-New Jersey Medical School, Newark (A.S., Y.I., S.S., D.K.Z., J.S.); Department of Cardiovascular Medicine and Hypertension, Graduate School of Medical and Dental Science, Kagoshima University, Japan (Y.I.); Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Rome, Italy (S.S.); and Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy (S.S.).
Yoshiyuki IkedaFrom the Department of Cell Biology and Molecular Medicine, Rutgers-New Jersey Medical School, Newark (A.S., Y.I., S.S., D.K.Z., J.S.); Department of Cardiovascular Medicine and Hypertension, Graduate School of Medical and Dental Science, Kagoshima University, Japan (Y.I.); Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Rome, Italy (S.S.); and Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy (S.S.).
Sebastiano SciarrettaFrom the Department of Cell Biology and Molecular Medicine, Rutgers-New Jersey Medical School, Newark (A.S., Y.I., S.S., D.K.Z., J.S.); Department of Cardiovascular Medicine and Hypertension, Graduate School of Medical and Dental Science, Kagoshima University, Japan (Y.I.); Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Rome, Italy (S.S.); and Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy (S.S.).
Daniela K ZablockiFrom the Department of Cell Biology and Molecular Medicine, Rutgers-New Jersey Medical School, Newark (A.S., Y.I., S.S., D.K.Z., J.S.); Department of Cardiovascular Medicine and Hypertension, Graduate School of Medical and Dental Science, Kagoshima University, Japan (Y.I.); Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Rome, Italy (S.S.); and Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy (S.S.).
Junichi SadoshimaFrom the Department of Cell Biology and Molecular Medicine, Rutgers-New Jersey Medical School, Newark (A.S., Y.I., S.S., D.K.Z., J.S.); Department of Cardiovascular Medicine and Hypertension, Graduate School of Medical and Dental Science, Kagoshima University, Japan (Y.I.); Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Rome, Italy (S.S.); and Department of AngioCardioNeurology, IRCCS Neuromed, Pozzilli, Italy (S.S.). sadoshju@njms.rutgers.edu.
Sapienza University of Rome · IT

Funding

Cysteine oxidation in the heartR01HL091469 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI Junichi Sadoshima · 2008 to 2026
$9.4M
The Role of Serine Signaling in Compensatory Cardiac HypertrophyR01HL112330 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI Junichi Sadoshima · 2012 to 2026
$7.5M
The Role of Thioredoxin in the Aging HeartR01AG023039 · NIA · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SADOSHIMA, JUNICHI · 2004 to 2018
$5.8M
Regulation of myocardial growth and death by GSK-3R01HL067724 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SADOSHIMA, JUNICHI · 2000 to 2018
$5.1M
Regulation of myocardial growth and death by autophagyR01HL102738 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SADOSHIMA, JUNICHI · 2010 to 2014
$2.5M
NHLBI NIH HHS R01 HL067724NHLBI NIH HHS R01 HL091469NHLBI NIH HHS R01 HL102738NHLBI NIH HHS R01 HL112330NIA NIH HHS R01 AG023039
6 · The paper itself

Abstract

The aging population is increasing in developed countries. Because the incidence of cardiac disease increases dramatically with age, it is important to understand the molecular mechanisms through which the heart becomes either more or less susceptible to stress. Cardiac aging is characterized by the presence of hypertrophy, fibrosis, and accumulation of misfolded proteins and dysfunctional mitochondria. Macroautophagy (hereafter referred to as autophagy) is a lysosome-dependent bulk degradation mechanism that is essential for intracellular protein and organelle quality control. Autophagy and autophagic flux are generally decreased in aging hearts, and murine autophagy loss-of-function models develop exacerbated cardiac dysfunction that is accompanied by the accumulation of misfolded proteins and dysfunctional organelles. On the contrary, stimulation of autophagy generally improves cardiac function in mouse models of protein aggregation by removing accumulated misfolded proteins, dysfunctional mitochondria, and damaged DNA, thereby improving the overall cellular environment and alleviating aging-associated pathology in the heart. Increasing lines of evidence suggest that autophagy is required for many mechanisms that mediate lifespan extension, such as caloric restriction, in various organisms. These results raise the exciting possibility that autophagy may play an important role in combating the adverse effects of aging in the heart. In this review, we discuss the role of autophagy in the heart during aging, how autophagy alleviates age-dependent changes in the heart, and how the level of autophagy in the aging heart can be restored.

Indexed as

AutophagyAgingAnimalsHumansMitophagyMyocardiumOxidative StressSignal Transductionagingautophagymitochondriamitochondrial degradationNADoxidative stress

Identifiers

PMID27174950
PMCPMC4869999
OpenAlexW2366061453

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.