ReviewAntioxidants (Basel, Switzerland)2019
Mitochondrial Genome (mtDNA) Mutations that Generate Reactive Oxygen Species.
Review in Antioxidants (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 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.
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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
85 citing papers in PubMed, 151 citations in OpenAlex.
- The Role of Skeletal Muscle Mitochondria in NLRP3 Inflammasome Signaling.Biomolecules · 2026Review
- Shifting the Balance: Mitochondrial Heteroplasmy as a Driver of Cardiac Disease.Circulation research · 2026Review
- Circulating Mitochondrial DNA Measures Across Malignancies: Diagnostic Accuracy and Prognostic Associations.Cancer medicine · 2026Article
- Oxidative stress biomarkers in assisted reproductive technologies: From follicular redox biology to clinical translation.Redox biology · 2026Review
- Small but mighty: mitochondrial DNA at the centre of retrograde signalling.Cell communication and signaling : CCS · 2026Review
- Mitochondrial DNA mutations and intercellular mitochondrial transfer in cancer: mechanisms, biological effects, and clinical potential.Biomarker research · 2026Review
- Mitochondrial Dysfunction Associated with mtDNA Mutation: Mitochondrial Genome Editing in Atherosclerosis Research.Current medicinal chemistry · 2026Article
- Pathogenic role of mitochondrial DNA mutations in heart failure: clinical features, mechanisms, and therapeutic prospects.Frontiers in cardiovascular medicine · 2026Review
- Mitochondrial retrograde signaling in gastric cancer: mtDNA mutations, ROS-driven NF-κB/HIF-1α activation, and Warburg effect amplification.Frontiers in physiology · 2026Review
- Oxidative stress and endoplasmic reticulum stress in acute kidney injury: mechanistic crosstalk and therapeutic modulation.Frontiers in medicine · 2026Review
- The microRNA miR-71 suppresses maladaptive UPRNature communications · 2025Article
- PSMD4 Alleviates Aβ₁₋₄₂-Induced Mitochondrial Dysfunction and Oxidative Stress via the PGC-1α/Nrf Axis in Alzheimer's Disease Models.Molecular neurobiology · 2025Article
- Mitonuclear Coevolution in Bumblebees (Bombus): Genomic Signatures and Its Role in Climatic Niche Adaptation.Genome biology and evolution · 2025Article
- Advances in the study of mechanisms underlying olfactory dysfunction in obstructive sleep apnea:a narrative review.Sleep and biological rhythms · 2025Review
- Diethyldithiocarbamate-CuNanomedicine (London, England) · 2025Article
- Investigating the genetic association of mitochondrial DNA copy number with neurodegenerative diseases.BMC neurology · 2025Article
- Mitochondrial DNA variants in the pathogenesis and metabolic alterations of diabetes mellitus.Molecular genetics and metabolism reports · 2025Review
- Identification of Ovarian High-Grade Serous Carcinoma with Mitochondrial Gene Variation.International journal of molecular sciences · 2025Article
- TMAO Induces Vascular Endothelial Cells Pyroptosis Through TET2-CYTB-ROS Pathway.Journal of inflammation research · 2025Article
- Pathogenic synergy: dysfunctional mitochondria and neuroinflammation in neurodegenerative diseases associated with aging.Frontiers in aging · 2025Review
25 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 1 institution in 1 country.
Funding
Abstract
Mitochondria are critical for the energetic demands of virtually every cellular process within nucleated eukaryotic cells. They harbour multiple copies of their own genome (mtDNA), as well as the protein-synthesing systems required for the translation of vital subunits of the oxidative phosphorylation machinery used to generate adenosine triphosphate (ATP). Molecular lesions to the mtDNA cause severe metabolic diseases and have been proposed to contribute to the progressive nature of common age-related diseases such as cancer, cardiomyopathy, diabetes, and neurodegenerative disorders. As a consequence of playing a central role in cellular energy metabolism, mitochondria produce reactive oxygen species (ROS) as a by-product of respiration. Here we review the evidence that mutations in the mtDNA exacerbate ROS production, contributing to disease.
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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.