Evidence map›Paper›PMID 26549356›Full record

ReviewJournal of molecular and cellular cardiology2016

Staying young at heart: autophagy and adaptation to cardiac aging.

Leonardo J Leon, Åsa B Gustafsson

Abstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

26 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Review
  3. ZnT6-mediated ZnMolecular and cellular biochemistry · 2025
    Article
  4. Upstream targeting for the prevention of atrial fibrillation: Targeting Risk Interventions and Metformin for Atrial Fibrillation (TRIM-AF)-rationale and study design.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2025
    Article
  5. Review
  6. The role of autophagy in the progression of HIV infected cardiomyopathy.Frontiers in cell and developmental biology · 2024
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. A Healthy Heart and a Healthy Brain: Looking at Mitophagy.Frontiers in cell and developmental biology · 2020
    Review
  15. Mitochondrial ROS-Modulated mtDNA: A Potential Target for Cardiac Aging.Oxidative medicine and cellular longevity · 2020
    Review
  16. HAging · 2019
    Article
  17. Article
  18. Article
  19. Article
  20. Article
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.

Leonardo J LeonSkaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, La Jolla, CA, United States.
Åsa B GustafssonSkaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, La Jolla, CA, United States. Electronic address: asag@ucsd.edu.
University of California, San Diego · US

Funding

Surgery, Physiology and ImmunohistopathologyP01HL085577 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI GLEMBOTSKI, CHRIS · 2006 to 2017
$18.4M
Role of Bnip3 in Myocardial Ischemia/ReperfusionR01HL087023 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUSTAFSSON, ASA B. · 2007 to 2016
$3.8M
NHLBI NIH HHS P01 HL085577NHLBI NIH HHS R01 HL087023
6 · The paper itself

Abstract

Aging is a predominant risk factor for developing cardiovascular disease. Therefore, the cellular processes that contribute to aging are attractive targets for therapeutic interventions that can delay or prevent the development of age-related diseases. Our understanding of the underlying mechanisms that contribute to the decline in cell and tissue functions with age has greatly advanced over the past decade. Classical hallmarks of aging cells include increased levels of reactive oxygen species, DNA damage, accumulation of dysfunctional organelles, oxidized proteins and lipids. These all contribute to a progressive decline in the normal physiological function of the cell and to the onset of age-related conditions. A major cause of the aging process is progressive loss of cellular quality control. Autophagy is an important quality control pathway and is necessary to maintain cardiac homeostasis and to adapt to stress. A reduction in autophagy has been observed in a number of aging models and there is compelling evidence that enhanced autophagy delays aging and extends life span. Enhancing autophagy counteracts age-associated accumulation of protein aggregates and damaged organelles in cells. In this review, we discuss the functional role of autophagy in maintaining homeostasis in the heart, and how a decline is associated with accelerated cardiac aging. We also evaluate therapeutic approaches being researched in an effort to maintain a healthy young heart.

Indexed as

Adaptation, PhysiologicalAgingAnimalsAutophagyCellular SenescenceGene Expression RegulationHeartHumansMyocardiumOxidation-ReductionOxidative StressSignal TransductionAgingAutophagyHeartMitochondria

Identifiers

PMID26549356
PMCPMC4860161
OpenAlexW2195213218

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.