Evidence map›Paper›PMID 26602750›Full record

ReviewJournal of molecular and cellular cardiology2016

Therapeutic targeting of autophagy in cardiovascular disease.

Gabriele G Schiattarella, Joseph A Hill

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 95 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

95 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Coenzyme QFrontiers in cardiovascular medicine · 2022
    Pooled it
  3. Pooled it
  4. Trial
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. SGLT2 inhibitors: how do they affect the cardiac cells.Molecular and cellular biochemistry · 2025
    Review
  12. Autophagy · 2025
    Article
  13. Article
  14. Review
  15. The Potential of Mesenchymal Stem Cell-Derived Exosomes in Cardiac Repair.International journal of molecular sciences · 2024
    Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review

35 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

2 authors.

Gabriele G SchiattarellaDepartments of Internal Medicine (Cardiology) and Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-8573, USA.
Joseph A HillDepartments of Internal Medicine (Cardiology) and Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-8573, USA. Electronic address: joseph.hill@utsouthwestern.edu.

Funding

Microenvironmental control of progenitors in organ dysfunction and repairU01HL100401 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI OLSON, ERIC N, SCHNEIDER, JAY W · 2009 to 2015
$8.3M
Training in Cardiovascular ResearchT32HL125247 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI JOSEPH A HILL · 2015 to 2026
$4.3M
STIM1: Master Regulator of Calcium Homeostasis in CardiomyocytesR01HL120732 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HILL, JOSEPH A · 2013 to 2016
$1.6M
Rodent Ultrasound Imaging SystemS10RR023729 · NCRR · UT SOUTHWESTERN MEDICAL CENTER · PI HILL, JOSEPH A · 2009 to 2009
$290k
NCRR NIH HHS S10 RR023729NHLBI NIH HHS R01 HL120732NHLBI NIH HHS T32 HL125247NHLBI NIH HHS U01 HL100401
6 · The paper itself

Abstract

Autophagy is an evolutionarily ancient process of intracellular catabolism necessary to preserve cellular homeostasis in response to a wide variety of stresses. In the case of post-mitotic cells, where cell replacement is not an option, finely tuned quality control of cytoplasmic constituents and organelles is especially critical. And due to the ubiquitous and critical role of autophagic flux in the maintenance of cell health, it comes as little surprise that perturbation of the autophagic process is observed in multiple disease processes. A large body of preclinical evidence suggests that autophagy is a double-edged sword in cardiovascular disease, acting in either beneficial or maladaptive ways, depending on the context. In light of this, the autophagic machinery in cardiomyocytes and other cardiovascular cell types has been proposed as a potential therapeutic target. Here, we summarize current knowledge regarding the dual functions of autophagy in cardiovascular disease. We go on to analyze recent evidence suggesting that titration of autophagic flux holds potential as a novel treatment strategy.

Indexed as

AutophagyMolecular Targeted TherapyAnimalsAntineoplastic AgentsApoptosisCardiovascular DiseasesHumansLysosomesMyocytes, CardiacRisk FactorsSignal TransductionTranslational Research, BiomedicalAntineoplastic AgentsCardiac hypertrophyHeart failureRemodeling

Identifiers

PMID26602750
PMCPMC4871782

What OpenQuestion holds

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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.