Evidence map›Paper›PMID 25593583›Full record

ReviewJournal of geriatric cardiology : JGC2014

The role and modulation of autophagy in experimental models of myocardial ischemia-reperfusion injury.

Carol Chen-Scarabelli, Pratik R Agrawal, Louis Saravolatz, Cadigia Abuniat, Gabriele Scarabelli, Anastasis Stephanou, Leena Loomba, Jagat Narula, Tiziano M Scarabelli, Richard Knight

Abstract readReview
In one paragraph

Review in Journal of geriatric cardiology : JGC, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

28 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Advances in the Protective Mechanism of NO, HFrontiers in cardiovascular medicine · 2020
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Balancing Autophagy for a Healthy Heart.Current opinion in physiology · 2018
    Article
  19. Article
  20. Divergent Effects of Cyclophilin-D Inhibition on the Female Rat Heart: Acute Versus Chronic Post-Myocardial Infarction.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2018
    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

10 authors at 1 institution in 1 country.

Carol Chen-ScarabelliVA Ann Arbor Health Care System, University of Michigan, 2215 Fuller Rd, Ann Arbor, MI 48105, USA.
Pratik R AgrawalZena and Michael A. Wiener Cardiovascular Institute, Mount Sinai Medical Center, One Gustave L. Levy Place, Box 1030, New York, NY 10029-6574, USA.
Louis SaravolatzSt John Hospital and Medical Center, Wayne State University School of Medicine, 22101 Moross Rd., Detroit, MI 48236, USA.
Cadigia AbuniatSt John Hospital and Medical Center, Wayne State University School of Medicine, 22101 Moross Rd., Detroit, MI 48236, USA.
Gabriele ScarabelliSt John Hospital and Medical Center, Wayne State University School of Medicine, 22101 Moross Rd., Detroit, MI 48236, USA.
Anastasis StephanouMedical and Molecular Biology Unit, University College London, UCL, 30 Guildford St., London, WC1N 1EH, UK.
Leena LoombaSt John Hospital and Medical Center, Wayne State University School of Medicine, 22101 Moross Rd., Detroit, MI 48236, USA.
Jagat NarulaZena and Michael A. Wiener Cardiovascular Institute, Mount Sinai Medical Center, One Gustave L. Levy Place, Box 1030, New York, NY 10029-6574, USA.
Tiziano M ScarabelliZena and Michael A. Wiener Cardiovascular Institute, Mount Sinai Medical Center, One Gustave L. Levy Place, Box 1030, New York, NY 10029-6574, USA ; St John Hospital and Medical Center, Wayne State University School of Medicine, 22101 Moross Rd., Detroit, MI 48236, USA.
Richard KnightMedical and Molecular Biology Unit, University College London, UCL, 30 Guildford St., London, WC1N 1EH, UK.
Wayne State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A physiological sequence called autophagy qualitatively determines cellular viability by removing protein aggregates and damaged cytoplasmic constituents, and contributes significantly to the degree of myocardial ischemia-reperfusion (I/R) injury. This tightly orchestrated catabolic cellular 'housekeeping' process provides cells with a new source of energy to adapt to stressful conditions. This process was first described as a pro-survival mechanism, but increasing evidence suggests that it can also lead to the demise of the cell. Autophagy has been implicated in the pathogenesis of multiple cardiac conditions including myocardial I/R injury. However, a debate persists as to whether autophagy acts as a protective mechanism or contributes to the injurious effects of I/R injury in the heart. This controversy may stem from several factors including the variability in the experimental models and species, and the methodology used to assess autophagy. This review provides updated knowledge on the modulation and role of autophagy in isolated cardiac cells subjected to I/R, and the growing interest towards manipulating autophagy to increase the survival of cardiac myocytes under conditions of stress-most notably being I/R injury. Perturbation of this evolutionarily conserved intracellular cleansing autophagy mechanism, by targeted modulation through, among others, mammalian target of rapamycin (mTOR) inhibitors, adenosine monophosphate-activated protein kinase (AMPK) modulators, calcium lowering agents, resveratrol, longevinex, sirtuin activators, the proapoptotic gene Bnip3, IP3 and lysosome inhibitors, may confer resistance to heart cells against I/R induced cell death. Thus, therapeutic manipulation of autophagy in the challenged myocardium may benefit post-infarction cardiac healing and remodeling.

Indexed as

AutophagyCell survivalHeartIschemia-reperfusion injury

Identifiers

PMID25593583
PMCPMC4294150
OpenAlexW2097001275

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.