Evidence map›Paper›PMID 35749842›Full record

ArticleRedox biology2022

Mitochondrial metabolism and bioenergetic function in an anoxic isolated adult mouse cardiomyocyte model of in vivo cardiac ischemia-reperfusion injury.

Anja V Gruszczyk, Alva M Casey, Andrew M James, Hiran A Prag, Nils Burger, Georgina R Bates, Andrew R Hall, Fay M Allen, Thomas Krieg, Kourosh Saeb-Parsy and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Redox biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.5field-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, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
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  7. Article
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  9. The Pro-Oncogenic Protein IFInternational journal of molecular sciences · 2023
    Article
  10. Review
  11. Article
  12. 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

11 authors at 1 institution in 1 country.

Anja V GruszczykMRC Mitochondrial Biology Unit, Biomedical Campus, University of Cambridge, Cambridge, CB2 0XY, UK; Department of Surgery and Cambridge NIHR Biomedical Research Centre, Biomedical Campus, University of Cambridge, Cambridge, CB2 2QQ, UK; NIHR Biomedical Research Centre and NIHR Blood and Transplant Research Unit in Organ Donation and Transplantation, Cambridge Biomedical Campus, Cambridge, UK.
Alva M CaseyMRC Mitochondrial Biology Unit, Biomedical Campus, University of Cambridge, Cambridge, CB2 0XY, UK.
Andrew M JamesMRC Mitochondrial Biology Unit, Biomedical Campus, University of Cambridge, Cambridge, CB2 0XY, UK.
Hiran A PragMRC Mitochondrial Biology Unit, Biomedical Campus, University of Cambridge, Cambridge, CB2 0XY, UK; Department of Medicine, University of Cambridge, Cambridge, CB2 0QQ, UK.
Nils BurgerMRC Mitochondrial Biology Unit, Biomedical Campus, University of Cambridge, Cambridge, CB2 0XY, UK.
Georgina R BatesMRC Mitochondrial Biology Unit, Biomedical Campus, University of Cambridge, Cambridge, CB2 0XY, UK.
Andrew R HallMRC Mitochondrial Biology Unit, Biomedical Campus, University of Cambridge, Cambridge, CB2 0XY, UK.
Fay M AllenMRC Mitochondrial Biology Unit, Biomedical Campus, University of Cambridge, Cambridge, CB2 0XY, UK.
Thomas KriegDepartment of Medicine, University of Cambridge, Cambridge, CB2 0QQ, UK.
Kourosh Saeb-ParsyDepartment of Surgery and Cambridge NIHR Biomedical Research Centre, Biomedical Campus, University of Cambridge, Cambridge, CB2 2QQ, UK; NIHR Biomedical Research Centre and NIHR Blood and Transplant Research Unit in Organ Donation and Transplantation, Cambridge Biomedical Campus, Cambridge, UK.
Michael P MurphyMRC Mitochondrial Biology Unit, Biomedical Campus, University of Cambridge, Cambridge, CB2 0XY, UK; Department of Medicine, University of Cambridge, Cambridge, CB2 0QQ, UK. Electronic address: mpm@mrc-mbu.cam.ac.uk.
University of Cambridge · GB

Funding

Department of HealthMedical Research Council MC_UU_00015/3Wellcome TrustWellcome Trust 220257/Z/20/Z
6 · The paper itself

Abstract

Cell models of cardiac ischemia-reperfusion (IR) injury are essential to facilitate understanding, but current monolayer cell models poorly replicate the in vivo IR injury that occurs within a three-dimensional tissue. Here we show that this is for two reasons: the residual oxygen present in many cellular hypoxia models sustains mitochondrial oxidative phosphorylation; and the loss of lactate from cells into the incubation medium during ischemia enables cells to sustain glycolysis. To overcome these limitations, we incubated isolated adult mouse cardiomyocytes anoxically while inhibiting lactate efflux. These interventions recapitulated key markers of in vivo ischemia, notably the accumulation of succinate and the loss of adenine nucleotides. Upon reoxygenation after anoxia the succinate that had accumulated during anoxia was rapidly oxidized in association with extensive mitochondrial superoxide/hydrogen peroxide production and cell injury, mimicking reperfusion injury. This cell model will enable key aspects of cardiac IR injury to be assessed in vitro.

Indexed as

Myocytes, CardiacReperfusion InjuryAnimalsDisease Models, AnimalEnergy MetabolismHypoxiaIschemiaLactatesMiceReactive Oxygen SpeciesSuccinic AcidLactatesReactive Oxygen SpeciesSuccinic AcidCardiomyocytesHydrogen peroxideIschemia-reperfusion injuryMetabolismMitochondria

Identifiers

PMID35749842
PMCPMC9234472
OpenAlexW4283018145

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.