ReviewBioscience reports2016
Combined defects in oxidative phosphorylation and fatty acid β-oxidation in mitochondrial disease.
Review in Bioscience reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
84 citing papers in PubMed, 1 synthesis or guideline pooled it, 146 citations in OpenAlex.
- A systematic review on the biochemical threshold of mitochondrial genetic variants.Genome research · 2024Pooled it
- Understanding the microRNA signature associated with Reye's syndrome.Protoplasma · 2026Review
- Downregulated ECHS1 and HADH-mediated fatty acid β-oxidation contributes to mitochondrial dysfunction in salivary glands of Sjögren's syndrome.Journal of translational autoimmunity · 2026Article
- Optical, Tomographic, and Mass Spectrometry Imaging Methods for Burn Wounds: Capabilities, Limitations, and Clinical Potential.Biomedicines · 2026Review
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- Metabolic Dysregulation in Laminopathies: Implications for Heart Failure and Cardiac Health.Current heart failure reports · 2026Review
- Glycolytic reprogramming impairs chondrocyte function in broilers with femoral head necrosis.The veterinary quarterly · 2025Article
- Investigating the Therapeutic Potential of miRNA-137-3p/383-5p/PGC-1α Signalling Nexus Against Cardiac Hypertrophy.Journal of cardiovascular translational research · 2025Article
- Targeting the FABP Axis: Interplay Between Lipid Metabolism, Neuroinflammation, and Neurodegeneration.Cells · 2025Review
- TNFα activation of the PLEKHA5-FCRLA axis disturbs lipid metabolism, leading to the progression of cutaneous malignant melanoma.Lipids in health and disease · 2025Article
- Hidden β-γ Dehydrogenation Products in Long-Chain Fatty Acid Oxidation Unveiled by NMR: Implications on Lipid Metabolism.ACS bio & med chem Au · 2025Article
- Hormonal Crossroads in Inborn Errors of the Metabolism Impact of Puberty and Dietary Interventions on Metabolic Health.Metabolites · 2025Review
- A novel polyribonucleotide nucleotidyltransferase 1 (Translational pediatrics · 2025Article
- Effects of atmospherically relevant PMFrontiers in public health · 2025Review
- Cardiomyopeptide-Regulated PPARγ Expression Plays a Critical Role in Maintaining Mitochondrial Integrity and Preventing Cardiac Ischemia/Reperfusion Injury.International journal of medical sciences · 2025Article
- Mitochondria associated membranes in dilated cardiomyopathy: connecting pathogenesis and cellular dysfunction.Frontiers in cardiovascular medicine · 2025Review
- Identification of DAP3 as candidate prognosis marker and potential therapeutic target for hepatocellular carcinoma.Frontiers in immunology · 2025Article
- Bioenergetic-related gene expression in the hippocampus predicts internalizing vs. externalizing behavior in an animal model of temperament.Frontiers in molecular neuroscience · 2025Article
- Spermidine Enhances Mitochondrial Bioenergetics in Young and Aged Human-Induced Pluripotent Stem Cell-Derived Neurons.Antioxidants (Basel, Switzerland) · 2024Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria provide the main source of energy to eukaryotic cells, oxidizing fats and sugars to generate ATP. Mitochondrial fatty acid β-oxidation (FAO) and oxidative phosphorylation (OXPHOS) are two metabolic pathways which are central to this process. Defects in these pathways can result in diseases of the brain, skeletal muscle, heart and liver, affecting approximately 1 in 5000 live births. There are no effective therapies for these disorders, with quality of life severely reduced for most patients. The pathology underlying many aspects of these diseases is not well understood; for example, it is not clear why some patients with primary FAO deficiencies exhibit secondary OXPHOS defects. However, recent findings suggest that physical interactions exist between FAO and OXPHOS proteins, and that these interactions are critical for both FAO and OXPHOS function. Here, we review our current understanding of the interactions between FAO and OXPHOS proteins and how defects in these two metabolic pathways contribute to mitochondrial disease pathogenesis.
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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.