Evidence map›Paper›PMID 28685325›Full record

ReviewThe journal of physiological sciences : JPS2017

Potential signaling pathways of acute endurance exercise-induced cardiac autophagy and mitophagy and its possible role in cardioprotection.

Youngil Lee, Insu Kwon, Yongchul Jang, Wankeun Song, Ludmila M Cosio-Lima, Mark H Roltsch

Erratum issuedAbstract readReview
In one paragraph

Review in The journal of physiological sciences : JPS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–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

16 citing papers in PubMed.

  1. Review
  2. Sage (Anatomy & cell biology · 2024
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Cardiac microtubules in health and heart disease.Experimental biology and medicine (Maywood, N.J.) · 2019
    Review
  12. Review
  13. Article
  14. Article
  15. Cardiac basal autophagic activity and increased exercise capacity.The journal of physiological sciences : JPS · 2018
    Article
  16. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Youngil LeeMolecular and Cellular Exercise Physiology Laboratory, Department of Exercise Science and Community Health, University of West Florida, 11000 University Parkway, Pensacola, FL, 32514, USA. ylee1@uwf.edu.
Insu KwonMolecular and Cellular Exercise Physiology Laboratory, Department of Exercise Science and Community Health, University of West Florida, 11000 University Parkway, Pensacola, FL, 32514, USA.
Yongchul JangMolecular and Cellular Exercise Physiology Laboratory, Department of Exercise Science and Community Health, University of West Florida, 11000 University Parkway, Pensacola, FL, 32514, USA.
Wankeun SongMolecular and Cellular Exercise Physiology Laboratory, Department of Exercise Science and Community Health, University of West Florida, 11000 University Parkway, Pensacola, FL, 32514, USA.
Ludmila M Cosio-LimaMolecular and Cellular Exercise Physiology Laboratory, Department of Exercise Science and Community Health, University of West Florida, 11000 University Parkway, Pensacola, FL, 32514, USA.
Mark H RoltschMolecular and Cellular Exercise Physiology Laboratory, Department of Exercise Science and Community Health, University of West Florida, 11000 University Parkway, Pensacola, FL, 32514, USA.

Funding

University of West Florida 164336University of West Florida CF6672
6 · The paper itself

Abstract

Cardiac myocytes are terminally differentiated cells and possess extremely limited regenerative capacity; therefore, preservation of mature cardiac myocytes throughout the individual's entire life span contributes substantially to healthy living. Autophagy, a lysosome-dependent cellular catabolic process, is essential for normal cardiac function and mitochondria maintenance. Therefore, it may be reasonable to hypothesize that if endurance exercise promotes cardiac autophagy and mitochondrial autophagy or mitophagy, exercise-induced cardiac autophagy (EICA) or exercise-induced cardiac mitophagy (EICM) may confer propitious cellular environment and thus protect the heart against detrimental stresses, such as an ischemia-reperfusion (I/R) injury. However, although the body of evidence supporting EICA and EICM is growing, the molecular mechanisms of EICA and EICM and their possible roles in cardioprotection against an I/R injury are poorly understood. Here, we introduce the general mechanisms of autophagy in an attempt to integrate potential molecular pathways of EICA and EICM and also highlight a potential insight into EICA and EICM in cardioprotection against an I/R insult.

Indexed as

AutophagyMitochondria, HeartMitophagyMyocytes, CardiacSignal TransductionAnimalsHumansAutophagyEndurance exerciseHeartIschemia reperfusionMitophagy

Identifiers

PMID28685325
PMCPMC5684252

What OpenQuestion holds

Textmetadata
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.