ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2016
Mitochondrial structure and function are not different between nonfailing donor and end-stage failing human hearts.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
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.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Loss of Rab8a-Dependent Tethering of Lipid Droplets to Mitochondria Contributes to Hypoxia-Reoxygenation Injury.MedComm · 2026Article
- A perspective on the future of heart failure research.Journal of molecular and cellular cardiology plus · 2026Article
- Cardiac intermediary metabolism in heart failure: substrate use, signalling roles and therapeutic targets.Nature reviews. Cardiology · 2025Review
- Comparison of the stage-dependent mitochondrial changes in response to pressure overload between the diseased right and left ventricle in the rat.Basic research in cardiology · 2024Article
- Human cardiac metabolism.Cell metabolism · 2024Review
- Lipotoxicity as a therapeutic target in obesity and diabetic cardiomyopathy.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2024Review
- The Janus-Faced Role of Lipid Droplets in Aging: Insights from the Cellular Perspective.Biomolecules · 2023Review
- Review
- Lipid Droplet-a New Target in Ischemic Heart Disease.Journal of cardiovascular translational research · 2022Review
- Plin5, a New Target in Diabetic Cardiomyopathy.Oxidative medicine and cellular longevity · 2022Review
- Pathophysiological Basis for Nutraceutical Supplementation in Heart Failure: A Comprehensive Review.Nutrients · 2021Review
- Article
- Impaired Myocardial Energetics Causes Mechanical Dysfunction in Decompensated Failing Hearts.Function (Oxford, England) · 2020Article
- Pathogenesis and pathophysiology of heart failure with reduced ejection fraction: translation to human studies.Heart failure reviews · 2019Review
- Reduced Myocardial Mitochondrial ROS Production in Mechanically Unloaded Hearts.Journal of cardiovascular translational research · 2019Article
- High-resolution respirometry in human endomyocardial biopsies shows reduced ventricular oxidative capacity related to heart failure.Experimental & molecular medicine · 2019Article
- Blossoming 20: The Energetic Regulator's Birthday Unveils its Versatility in Cardiac Diseases.Theranostics · 2019Review
- Engineering cardiac microphysiological systems to model pathological extracellular matrix remodeling.American journal of physiology. Heart and circulatory physiology · 2018Review
- Deciphering the Role of Lipid Droplets in Cardiovascular Disease: A Report From the 2017 National Heart, Lung, and Blood Institute Workshop.Circulation · 2018Review
- Heart failure-induced activation of phospholipase iPLAThe Journal of biological chemistry · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
During human heart failure, the balance of cardiac energy use switches from predominantly fatty acids (FAs) to glucose. We hypothesized that this substrate shift was the result of mitochondrial degeneration; therefore, we examined mitochondrial oxidation and ultrastructure in the failing human heart by using respirometry, transmission electron microscopy, and gene expression studies of demographically matched donor and failing human heart left ventricular (LV) tissues. Surprisingly, respiratory capacities for failing LV isolated mitochondria (n = 9) were not significantly diminished compared with donor LV isolated mitochondria (n = 7) for glycolysis (pyruvate + malate)- or FA (palmitoylcarnitine)-derived substrates, and mitochondrial densities, assessed via citrate synthase activity, were consistent between groups. Transmission electron microscopy images also showed no ultrastructural remodeling for failing vs. donor mitochondria; however, the fraction of lipid droplets (LDs) in direct contact with a mitochondrion was reduced, and the average distance between an LD and its nearest neighboring mitochondrion was increased. Analysis of FA processing gene expression between donor and failing LVs revealed 0.64-fold reduced transcript levels for the mitochondrial-LD tether, perilipin 5, in the failing myocardium (P = 0.003). Thus, reduced FA use in heart failure may result from improper delivery, potentially via decreased perilipin 5 expression and mitochondrial-LD tethering, and not from intrinsic mitochondrial dysfunction.-Holzem, K. M., Vinnakota, K. C., Ravikumar, V. K., Madden, E. J., Ewald, G. A., Dikranian, K., Beard, D. A., Efimov, I. R. Mitochondrial structure and function are not different between nonfailing donor and end-stage failing human hearts.
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Registered trials
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.