Evidence map›Paper›PMID 32587298›Full record

Trial reportScientific reports2020

Cardioprotective effect of succinate dehydrogenase inhibition in rat hearts and human myocardium with and without diabetes mellitus.

Nichlas Riise Jespersen, Marie Vognstoft Hjortbak, Thomas Ravn Lassen, Nicolaj Brejnholt Støttrup, Jacob Johnsen, Pernille Tilma Tonnesen, Steen Larsen, Hans-Henrik Kimose, Hans Erik Bøtker

Open access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

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  12. Complex II Biology in Aging, Health, and Disease.Antioxidants (Basel, Switzerland) · 2023
    Review
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  20. Citric Acid Cycle Metabolites Predict Infarct Size inInternational journal of molecular sciences · 2021
    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

9 authors at 2 institutions in 2 countries.

Nichlas Riise JespersenDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark. n.riise.jespersen@clin.au.dk.
Marie Vognstoft HjortbakDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Thomas Ravn LassenDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Nicolaj Brejnholt StøttrupDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Jacob JohnsenDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Pernille Tilma TonnesenDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Steen LarsenXlab, Center for Healthy Aging, Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark.
Hans-Henrik KimoseDepartment of Cardiothoracic Surgery, Aarhus University Hospital, Aarhus, Denmark.
Hans Erik BøtkerDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Aarhus University Hospital · DKUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemia reperfusion (IR) injury may be attenuated through succinate dehydrogenase (SDH) inhibition by dimethyl malonate (DiMAL). Whether SDH inhibition yields protection in diabetic individuals and translates into human cardiac tissue remain unknown. In isolated perfused hearts from 24 weeks old male Zucker diabetic fatty (ZDF) and age matched non-diabetic control rats and atrial trabeculae from patients with and without diabetes, we compared infarct size, contractile force recovery and mitochondrial function. The cardioprotective effect of a 10 minutes DiMAL administration prior to global ischemia and ischemic preconditioning (IPC) was evaluated. In non-diabetic hearts exposed to IR, DiMAL 0.1 mM reduced infarct size compared to IR (55 ± 7% vs. 69 ± 6%, p < 0.05). Mitochondrial respiration was reduced by DiMAL 0.6 mM compared to sham and DiMAL 0.1 mM (p < 0.05). In diabetic hearts an increased concentration of DiMAL (0.6 mM) was required for protection compared to IR (64 ± 13% vs. 79 ± 8%, p < 0.05). Mitochondrial function remained unchanged. In trabeculae from humans without diabetes, IPC and DiMAL improved contractile force recovery compared to IR (43 ± 12% and 43 ± 13% vs. 23 ± 13%, p < 0.05) but in patients with diabetes only IPC provided protection compared to IR (51 ± 15% vs. 21 ± 8%, p < 0.05). Neither IPC nor DiMAL modulated mitochondrial respiration in patients. Cardioprotection by SDH inhibition is possible in human tissue, but depends on diabetes status. The narrow therapeutic range and discrepancy in respiration between experimental and human studies may limit clinical translation.

Indexed as

AgedAnimalsCardiotonic AgentsDiabetes Mellitus, Type 2FemaleHeartHumansIschemic Preconditioning, MyocardialIsolated Heart PreparationMaleMalonatesMiddle AgedMitochondriaMyocardial ContractionMyocardial InfarctionMyocardial Reperfusion InjuryCardiotonic AgentsMalonatesmethyl malonateSDHD protein, humanSuccinate Dehydrogenase

Identifiers

PMID32587298
PMCPMC7316713
OpenAlexW3037503266

What OpenQuestion holds

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Registered trials

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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.