Evidence map›Paper›PMID 31409351›Full record

ArticleJournal of translational medicine2019

Renal temperature reduction progressively favors mitochondrial ROS production over respiration in hypothermic kidney preservation.

Koen D W Hendriks, Isabel M A Brüggenwirth, Hanno Maassen, Albert Gerding, Barbara Bakker, Robert J Porte, Robert H Henning, Henri G D Leuvenink

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 61 citations in OpenAlex.

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  17. Mitochondrial dysfunction in a rat model and the related risk of metabolic disorders.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2023
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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

8 authors at 1 institution in 1 country.

Koen D W HendriksDepartment of Clinical Pharmacy and Pharmacology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, 9713JZ, Groningen, The Netherlands. k.d.w.hendriks@umcg.nl.ORCID 0000-0002-1202-0389
Isabel M A BrüggenwirthSection of Hepatobiliary Surgery and Liver Transplantation, Department of Surgery, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Hanno MaassenDepartment of Surgery, University Medical Center Groningen, Groningen, The Netherlands.
Albert GerdingDepartment of Laboratory Medicine, University Medical Center Groningen, Groningen, The Netherlands.
Barbara BakkerDepartment of Pediatrics, University Medical Center Groningen, Groningen, The Netherlands.
Robert J PorteSection of Hepatobiliary Surgery and Liver Transplantation, Department of Surgery, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Robert H HenningDepartment of Clinical Pharmacy and Pharmacology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, 9713JZ, Groningen, The Netherlands.
Henri G D LeuveninkDepartment of Surgery, University Medical Center Groningen, Groningen, The Netherlands.
University Medical Center Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHypothermia, leading to mitochondrial inhibition, is widely used to reduce ischemic injury during kidney preservation. However, the exact effect of hypothermic kidney preservation on mitochondrial function remains unclear.

methodsWe evaluated mitochondrial function [i.e. oxygen consumption and production of reactive oxygen species (ROS)] in different models (porcine kidney perfusion, isolated kidney mitochondria, and HEK293 cells) at temperatures ranging 7-37 °C.

resultsLowering temperature in perfused kidneys and isolated mitochondria resulted in a rapid decrease in oxygen consumption (65% at 27 °C versus 20% at 7 °C compared to normothermic). Decreased oxygen consumption at lower temperatures was accompanied by a reduction in mitochondrial ROS production, albeit markedly less pronounced and amounting only 50% of normothermic values at 7 °C. Consequently, malondialdehyde (a marker of ROS-induced lipid peroxidation) accumulated in cold stored kidneys. Similarly, low temperature incubation of kidney cells increased lipid peroxidation, which is due to a loss of ROS scavenging in the cold.

conclusionsLowering of temperature highly affects mitochondrial function, resulting in a progressive discrepancy between the lowering of mitochondrial respiration and their production of ROS, explaining the deleterious effects of hypothermia in transplantation procedures. These results highlight the necessity to develop novel strategies to decrease the formation of ROS during hypothermic organ preservation.

Indexed as

Hypothermia, InducedOrgan PreservationRespirationTemperatureAnimalsAntioxidantsHEK293 CellsHumansHydrogen PeroxideKidneyMitochondriaOxygen ConsumptionReactive Oxygen SpeciesSwineAntioxidantsHydrogen PeroxideReactive Oxygen SpeciesHypothermic preservationKidney transplantationMachine perfusionMitochondrial functionReactive oxygen species

Identifiers

PMID31409351
PMCPMC6693148
OpenAlexW2968101426

What Socratic 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 Socratic graph.