Evidence map›Paper›PMID 29660243›Full record

ReviewActa physiologica (Oxford, England)2018

Autophagy-A key pathway for cardiac health and longevity.

B P Woodall, Å B Gustafsson

Open access · greenAbstract readReview
In one paragraph

Review in Acta physiologica (Oxford, England), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

27 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Review
  3. Berberine Extends Lifespan inAntioxidants (Basel, Switzerland) · 2025
    Article
  4. Review
  5. Article
  6. Autophagy Behavior under Local Hypothermia in Myocardiocytes Injury.Cardiovascular & hematological agents in medicinal chemistry · 2024
    Review
  7. Article
  8. Review
  9. Article
  10. Cardiovascular aging: the mitochondrial influence.The journal of cardiovascular aging · 2023
    Article
  11. Article
  12. Article
  13. Enhanced autophagy inAutophagy · 2022
    Article
  14. Article
  15. Ononin alleviates HExperimental and therapeutic medicine · 2021
    Article
  16. Article
  17. Review
  18. Article
  19. Reversible Treatment of Pressure Overload-Induced Left Ventricular Hypertrophy throughAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021
    Article
  20. Review
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

2 authors at 1 institution in 1 country.

B P WoodallSkaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, La Jolla, CA, USA.
Å B GustafssonSkaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, La Jolla, CA, USA.ORCID 0000-0001-6347-8210
University of California San Diego · US

Funding

Role of Bnip3 in Myocardial Ischemia/ReperfusionR01HL087023 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUSTAFSSON, ASA B. · 2007 to 2016
$3.8M
MCL-1 is a critical regulator of mitochondrial dynamics and function in myocytesR01HL132300 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUSTAFSSON, ASA B. · 2017 to 2020
$1.7M
Role of the Endosomal-Lysosomal Pathway in Mitochondrial Quality ControlR01HL138560 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUSTAFSSON, ASA B. · 2017 to 2020
$1.6M
Mitochondrial Quality Control in the Aging MyocardiumR21AG052280 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUSTAFSSON, ASA B. · 2016 to 2017
$426k
NHLBI NIH HHS R01 HL087023NHLBI NIH HHS R01 HL132300NHLBI NIH HHS R01 HL138560NIA NIH HHS R21 AG052280
6 · The paper itself

Abstract

As average life expectancy continues to rise in the developed world, age-associated pathologies are increasing in prevalence. The hallmarks of cardiac ageing include cardiomyocyte loss, fibrosis and hypertrophy, all of which contribute to an increased incidence of cardiac disease. At the molecular level, cellular ageing is characterized by increased ROS production, mitochondrial dysfunction and the accumulation of damaged proteins and organelles. Cardiomyocytes and other senescent cell types rely upon autophagy, a lysosome-mediated degradation pathway, to remove potentially toxic protein aggregates and damaged organelles from the cellular milieu. However, increasing lines of evidence point to an age-associated decrease in cardiomyocyte autophagy, with predictably negative consequences for cardiac function and health. Conversely, stimulation of autophagy has been shown to improve cellular health and cardiac function and to increase lifespan in numerous model organisms. Clearly, autophagy represents a critical pathway for cellular vitality, as well as a promising therapeutic target for the treatment of age-related cardiac pathologies. In this review, we will discuss the mechanism of autophagy and its regulation in the cell, the role of autophagy in the ageing heart, and how the autophagy pathway might be targeted to improve cardiac health.

Indexed as

AutophagyAge FactorsAgingAnimalsAutophagy-Related ProteinsCardiovascular AgentsCardiovascular DiseasesHumansLongevityMitochondria, HeartMitophagyMyocytes, CardiacRisk FactorsRisk Reduction BehaviorSignal TransductionAutophagy-Related ProteinsCardiovascular Agentsageingautophagyheart

Identifiers

PMID29660243
PMCPMC6527442
OpenAlexW2800119026

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.