Evidence map›Paper›PMID 23415552›Full record

ArticleJournal of the American College of Surgeons2013

Activation of the homeostatic intracellular repair response during cardiac surgery.

Salik M Jahania, David Sengstock, Peter Vaitkevicius, Allen Andres, Bruce R Ito, Roberta A Gottlieb, Robert M Mentzer

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in Journal of the American College of Surgeons, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03638609 (The Effect of Intra Aortic Balloon Pump Early Insertion on Mortality in Post Cardiac Arrest Patients With Acute Coronary Syndrome), which is not on this map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
3.1field-weighted citation impact, top 9% 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.

NCT03638609 naunknown statusnot on this mapstarted 2017, after this paper: background citation

The Effect of Intra Aortic Balloon Pump Early Insertion on Mortality in Post Cardiac Arrest Patients With Acute Coronary Syndrome

TypeinterventionalSponsorIndonesia UniversityRan2017 to 2018Enrolled102ConditionsPost-Cardiac Arrest SyndromeArmsIntra Aortic Balloon Pump
3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 40 citations in OpenAlex.

  1. Guideline
  2. Guideline
  3. Trial
  4. Review
  5. Mitophagy for cardioprotection.Basic research in cardiology · 2023
    Review
  6. Regulation of autophagy of the heart in ischemia and reperfusion.Apoptosis : an international journal on programmed cell death · 2023
    Review
  7. Article
  8. Mitophagy in Cardiovascular Diseases.Journal of clinical medicine · 2020
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. This old heart: Cardiac aging and autophagy.Journal of molecular and cellular cardiology · 2015
    Review
  18. Review
  19. Article
  20. Resveratrol regulates autophagy signaling in chronically ischemic myocardium.The Journal of thoracic and cardiovascular surgery · 2014
    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

7 authors at 2 institutions in 1 country.

Salik M JahaniaDepartment of Surgery, Wayne State University School of Medicine, Detroit, MI, USA.
David Sengstock
Peter Vaitkevicius
Allen Andres
Bruce R Ito
Roberta A Gottlieb
Robert M Mentzer
San Diego State University · USWayne State University · US

Funding

Autophagy, Adenosine and Pyruvate Protection During Heart SurgeryR01HL034579 · NHLBI · WAYNE STATE UNIVERSITY · PI GOTTLIEB, ROBERTA A., MENTZER, ROBERT M · 1985 to 2012
$4.1M
Rescue and Role of Complex I in myocardial ischemic injuryR01HL060590 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI GOTTLIEB, ROBERTA A. · 1998 to 2011
$3.6M
NHLBI NIH HHS 2R01 HL034579-25NHLBI NIH HHS 2R01 HL060590-15NHLBI NIH HHS R01 HL034579NHLBI NIH HHS R01 HL060590
6 · The paper itself

Abstract

backgroundThe homeostatic intracellular repair response (HIR2) is an endogenous beneficial pathway that eliminates damaged mitochondria and dysfunctional proteins in response to stress. The underlying mechanism is adaptive autophagy. The purpose of this study was to determine whether the HIR2 response is activated in the heart in patients undergoing cardiac surgery and to assess whether it is associated with the duration of ischemic arrest and predicted surgical outcomes. STUDY

designAutophagy was assessed in 19 patients undergoing coronary artery bypass or valve surgery requiring cardiopulmonary bypass. Biopsies of the right atrial appendage obtained before initiation of cardiopulmonary bypass and after weaning from cardiopulmonary bypass were analyzed for autophagy by immunoblotting for LC3, Beclin-1, autophagy 5-12, and p62. Changes in p62, a marker of autophagic flux, were correlated with duration of ischemia and with the mortality/morbidity risk scores obtained from the Society of Thoracic Surgeons Adult Cardiac Surgery Database (version 2.73).

resultsHeart surgery was associated with a robust increase in autophagic flux indicated by depletion of LC3-I, LC3-II, Beclin-1, and autophagy 5-12; the magnitude of change for each of these factors correlated significantly with changes in the flux marker p62. In addition, changes in p62 correlated directly with cross-clamp time and inversely with the mortality and morbidity risk scores.

conclusionsThese findings are consistent with preclinical studies indicating that HIR2 is cardioprotective and reveal that it is activated in patients in response to myocardial ischemic stress. Strategies designed to amplify HIR2 during conditions of cardiac stress might have a therapeutic use and represent an entirely new approach to myocardial protection in patients undergoing heart surgery.

Indexed as

AutophagyCardiac Surgical ProceduresHomeostasisFemaleHumansIntracellular Signaling Peptides and ProteinsMaleMiddle AgedMyocardiumIntracellular Signaling Peptides and Proteins

Identifiers

PMID23415552
PMCPMC3724756
OpenAlexW2046216514

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Registered trials

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.