Evidence map›Paper›PMID 27199126›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2016

Selective downregulation of mitochondrial electron transport chain activity and increased oxidative stress in human atrial fibrillation.

Larisa Emelyanova, Zain Ashary, Milanka Cosic, Ulugbek Negmadjanov, Gracious Ross, Farhan Rizvi, Susan Olet, David Kress, Jasbir Sra, A Jamil Tajik and 3 more

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

51 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
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  6. Mitochondrial Dysfunction in Cardiac Surgery.Anesthesiology clinics · 2025
    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

13 authors at 2 institutions in 1 country.

Larisa EmelyanovaSheikh Khalifa bin Hamad Al Thani Center for Integrative Research on Cardiovascular Aging, Aurora Sinai/Aurora St. Luke's Medical Centers, Milwaukee, Wisconsin;
Zain AsharySheikh Khalifa bin Hamad Al Thani Center for Integrative Research on Cardiovascular Aging, Aurora Sinai/Aurora St. Luke's Medical Centers, Milwaukee, Wisconsin;
Milanka CosicSheikh Khalifa bin Hamad Al Thani Center for Integrative Research on Cardiovascular Aging, Aurora Sinai/Aurora St. Luke's Medical Centers, Milwaukee, Wisconsin;
Ulugbek NegmadjanovSheikh Khalifa bin Hamad Al Thani Center for Integrative Research on Cardiovascular Aging, Aurora Sinai/Aurora St. Luke's Medical Centers, Milwaukee, Wisconsin;
Gracious RossSheikh Khalifa bin Hamad Al Thani Center for Integrative Research on Cardiovascular Aging, Aurora Sinai/Aurora St. Luke's Medical Centers, Milwaukee, Wisconsin;
Farhan RizviSheikh Khalifa bin Hamad Al Thani Center for Integrative Research on Cardiovascular Aging, Aurora Sinai/Aurora St. Luke's Medical Centers, Milwaukee, Wisconsin;
Susan OletPatient-Centered Research, Aurora Research Institute, Aurora Health Care, Milwaukee, Wisconsin; and.
David KressAurora Cardiovascular Services, Aurora Sinai/Aurora St. Luke's Medical Centers, Milwaukee, Wisconsin.
Jasbir SraAurora Cardiovascular Services, Aurora Sinai/Aurora St. Luke's Medical Centers, Milwaukee, Wisconsin.
A Jamil TajikAurora Cardiovascular Services, Aurora Sinai/Aurora St. Luke's Medical Centers, Milwaukee, Wisconsin.
Ekhson L HolmuhamedovSheikh Khalifa bin Hamad Al Thani Center for Integrative Research on Cardiovascular Aging, Aurora Sinai/Aurora St. Luke's Medical Centers, Milwaukee, Wisconsin;
Yang ShiSheikh Khalifa bin Hamad Al Thani Center for Integrative Research on Cardiovascular Aging, Aurora Sinai/Aurora St. Luke's Medical Centers, Milwaukee, Wisconsin;
Arshad JahangirSheikh Khalifa bin Hamad Al Thani Center for Integrative Research on Cardiovascular Aging, Aurora Sinai/Aurora St. Luke's Medical Centers, Milwaukee, Wisconsin; Patient-Centered Research, Aurora Research Institute, Aurora Health Care, Milwaukee, Wisconsin; and Aurora Cardiovascular Services, Aurora Sinai/Aurora St. Luke's Medical Centers, Milwaukee, Wisconsin publishing44@aurora.org.
Aurora St. Luke's Medical Center · USAurora Health Care · US

Funding

Mitochondrial Dysfunction and Susceptibility to Atrial Fibrillation in the ElderlR01HL101240 · NHLBI · MAYO CLINIC ARIZONA · PI JAHANGIR, ARSHAD · 2010 to 2013
$2.3M
Human Senescence and CardioprotectionR01HL089542 · NHLBI · MAYO CLINIC ROCHESTER · PI JAHANGIR, ARSHAD · 2008 to 2011
$1.6M
NHLBI NIH HHS R01 HL089542NHLBI NIH HHS R01 HL101240
6 · The paper itself

Abstract

Mitochondria are critical for maintaining normal cardiac function, and a deficit in mitochondrial energetics can lead to the development of the substrate that promotes atrial fibrillation (AF) and its progression. However, the link between mitochondrial dysfunction and AF in humans is still not fully defined. The aim of this study was to elucidate differences in the functional activity of mitochondrial oxidative phosphorylation (OXPHOS) complexes and oxidative stress in right atrial tissue from patients without (non-AF) and with AF (AF) who were undergoing open-heart surgery and were not significantly different for age, sex, major comorbidities, and medications. The overall functional activity of the electron transport chain (ETC), NADH:O2 oxidoreductase activity, was reduced by 30% in atrial tissue from AF compared with non-AF patients. This was predominantly due to a selective reduction in complex I (0.06 ± 0.007 vs. 0.09 ± 0.006 nmol·min(-1)·citrate synthase activity(-1), P = 0.02) and II (0.11 ± 0.012 vs. 0.16 ± 0.012 nmol·min(-1)·citrate synthase activity(-1), P = 0.003) functional activity in AF patients. Conversely, complex V activity was significantly increased in AF patients (0.21 ± 0.027 vs. 0.12 ± 0.01 nmol·min(-1)·citrate synthase activity(-1), P = 0.005). In addition, AF patients exhibited a higher oxidative stress with increased production of mitochondrial superoxide (73 ± 17 vs. 11 ± 2 arbitrary units, P = 0.03) and 4-hydroxynonenal level (77.64 ± 30.2 vs. 9.83 ± 2.83 ng·mg(-1) protein, P = 0.048). Our findings suggest that AF is associated with selective downregulation of ETC activity and increased oxidative stress that can contribute to the progression of the substrate for AF.

Indexed as

Oxidative PhosphorylationOxidative StressAgedAged, 80 and overAldehydesAtrial FibrillationCase-Control StudiesDisease ProgressionDown-RegulationElectron Transport Chain Complex ProteinsFemaleHeart AtriaHumansMaleMiddle AgedMitochondria, Heart4-hydroxy-2-nonenalAldehydesElectron Transport Chain Complex ProteinsSuperoxides4-hydroxynonenal protein adductsatrial fibrillationelectron transport chain complexeshumansmitochondriaoxidative phosphorylationoxidative stresssuperoxide

Identifiers

PMID27199126
PMCPMC4967212
OpenAlexW2346934269

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.