Evidence map›Paper›PMID 26472730›Full record

ArticleMolecular and cellular biochemistry2016

Effects of mild hyperhomocysteinemia on electron transport chain complexes, oxidative stress, and protein expression in rat cardiac mitochondria.

Veronika Timkova, Zuzana Tatarkova, Jan Lehotsky, Peter Racay, Dusan Dobrota, Peter Kaplan

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

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  10. Article
  11. Homocysteine and Mitochondria in Cardiovascular and Cerebrovascular Systems.International journal of molecular sciences · 2020
    Review
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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 1 institution in 1 country.

Veronika TimkovaDepartment of Medical Biochemistry, Jessenius Faculty of Medicine, Comenius University in Bratislava, Mala Hora 4, 036 01, Martin, Slovak Republic.
Zuzana TatarkovaDepartment of Medical Biochemistry, Jessenius Faculty of Medicine, Comenius University in Bratislava, Mala Hora 4, 036 01, Martin, Slovak Republic.
Jan LehotskyDepartment of Medical Biochemistry, Jessenius Faculty of Medicine, Comenius University in Bratislava, Mala Hora 4, 036 01, Martin, Slovak Republic.
Peter RacayDepartment of Medical Biochemistry, Jessenius Faculty of Medicine, Comenius University in Bratislava, Mala Hora 4, 036 01, Martin, Slovak Republic.
Dusan DobrotaDepartment of Medical Biochemistry, Jessenius Faculty of Medicine, Comenius University in Bratislava, Mala Hora 4, 036 01, Martin, Slovak Republic.
Peter KaplanDepartment of Medical Biochemistry, Jessenius Faculty of Medicine, Comenius University in Bratislava, Mala Hora 4, 036 01, Martin, Slovak Republic. kaplan@jfmed.uniba.sk.
Comenius University Bratislava · SK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperhomocysteinemia (HHcy) is an independent risk factor of cardiovascular disease, but the mechanisms of tissue injury are poorly understood. In the present study, we investigated the effect of HHcy on rat heart function, activities electron transport chain (ETC) complexes, mitochondrial protein expression, and protein oxidative damage. HHcy was induced by subcutaneous injection of Hcy (0.45 μmol/g of body weight) twice a day for a period of 2 weeks. Performance of hearts excised after the Hcy treatment was examined according to the Langendorff method at a constant pressure. Left ventricular developed pressure, as well as maximal rates of contraction (+dP/dt) and relaxation (-dP/dt), was significantly depressed in HHcy rats. HHcy was accompanied by significant inhibition of ETC complexes II-IV, whereas activity of the complex I was unchanged. The decline in ETC activities was not associated with elevated protein oxidative damage, as indicated by unchanged protein carbonyl, thiol, and dityrosine contents. Moreover, the level of protein adducts with 4-hydroxynonenal was decreased in HHcy rats. Additionally, 2D-gel electrophoresis with matrix-assisted laser desorption/ionization time-of-flight mass spectrometry did not show alterations in contents of inhibited ETC complexes. However, mass spectrometry analyses identified 8 proteins whose expression was significantly increased by HHcy. These proteins are known to play important roles in the cellular stress response, bioenergetics, and redox balance. Altogether, the results suggest that oxidative damage and altered protein expression are not possible causes of ETC dysfunction in HHcy rats. Increased expression of the other mitochondrial proteins indicates a protective response to Hcy-induced myocardial injury.

Indexed as

Oxidative StressAnimalsElectron TransportHeart Function TestsHyperhomocysteinemiaMaleMitochondria, HeartMitochondrial ProteinsRatsRats, WistarMitochondrial ProteinsElectron transport chainHeartHomocysteineMitochondriaOxidative stressProtein expression

Identifiers

PMID26472730
OpenAlexW2186558332

What OpenQuestion holds

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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.