Evidence map›Paper›PMID 27164961›Full record

ReviewJournal of cardiovascular translational research2016

The Critical Role of Bioenergetics in Donor Cardiac Allograft Preservation.

David A Schipper, Katherine M Marsh, Alice S Ferng, Dirk J Duncker, Jon D Laman, Zain Khalpey

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Journal of cardiovascular translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
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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

6 authors at 3 institutions in 2 countries.

David A SchipperDepartment of Surgery, Division of Cardiothoracic Surgery, University of Arizona College of Medicine, 1501 North Campbell Avenue, Room 4302, Tucson, AZ, 85724, USA.
Katherine M MarshDepartment of Surgery, Division of Cardiothoracic Surgery, University of Arizona College of Medicine, 1501 North Campbell Avenue, Room 4302, Tucson, AZ, 85724, USA.
Alice S FerngDepartment of Surgery, Division of Cardiothoracic Surgery, University of Arizona College of Medicine, 1501 North Campbell Avenue, Room 4302, Tucson, AZ, 85724, USA.
Dirk J DunckerDivision of Cardiology, Thoraxcenter Erasmus University Medical Center, Rotterdam, Netherlands.
Jon D LamanDepartment of Neuroscience, University Medical Center Groningen, Groningen, Netherlands.
Zain KhalpeyDepartment of Surgery, Division of Cardiothoracic Surgery, University of Arizona College of Medicine, 1501 North Campbell Avenue, Room 4302, Tucson, AZ, 85724, USA. zkhalpey@surgery.arizona.edu.
University of Arizona · USErasmus MC · NLUniversity Medical Center Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The traditional philosophy of ex vivo organ preservation has been to limit metabolic activity by storing organs in hypothermic, static conditions. This methodology cannot provide longevity of hearts for more than 4-6 h and is thereby insufficient to expand the number of available organs. Albeit at lower rate, the breakdown of ATP still occurs during hypothermia. Furthermore, cold static preservation does not prevent the permanent damage that occurs upon reperfusion known as ischemia-reperfusion (IR) injury. This damage is caused by increased reactive oxygen species (ROS) production in combination with mitochondrial permeability transition pore (mPTP) opening, highlighting the importance of mitochondria in ischemic storage. There has recently been a major paradigm shift in the field, with emerging research supporting changes in traditional storage approaches. Novel research suggests achieving metabolic homeostasis instead of attempting to limit metabolic activity which reduces IR injury and improves graft preservation. Maintaining high ATP levels and circumventing cold organ storage would be a much more sophisticated standard for organ storage and should be the focus of future research in organ preservation. Given the link between mPTP, Ca2(+), and ROS, managing Ca2(+) influx into the mitochondria during conditioning might be the next critical step towards preventing irreversible IR injury.

Indexed as

Energy MetabolismAdenosine TriphosphateAllograftsAnimalsCalcium SignalingCold IschemiaCold TemperatureHeart TransplantationHumansMitochondria, HeartMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMyocardial Reperfusion InjuryMyocardiumOrgan PreservationOrgan Preservation SolutionsAdenosine TriphosphateMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreOrgan Preservation SolutionsReactive Oxygen SpeciesBioenergeticsMitochondriaPreservationReactive oxygen speciesTransplant

Identifiers

PMID27164961
OpenAlexW2391905582

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.