ReviewMitochondrion2014
ATP/ADP ratio, the missed connection between mitochondria and the Warburg effect.
Review in Mitochondrion, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.
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
105 citing papers in PubMed, 179 citations in OpenAlex.
- Diaphragmatic Mitochondrial Myopathy in a Patient-Derived Mouse Model of Barth Syndrome.Journal of developmental biology · 2026Article
- Review
- Spinal cord injury induces mitochondrial dysfunction and metabolic reprogramming in non-regenerativeiScience · 2026Article
- ATP binding to lysozyme and superfolder GFP amyloid fibrils induces aggregate remodeling and attenuates their cytotoxicity.Cell death discovery · 2026Article
- Anti-cancer drugs targeting the NADH-binding site of VDAC rewire channel electrophysiology and partially suppress cation selectivity.The FEBS journal · 2026Article
- Itraconazole as a repurposed anti-cancer agent: focusing on synthesis, mechanisms of action and therapeutic insights.RSC advances · 2026Review
- The oncogenic CCDC6-RET fusion protein is a dual ATP- and ADP-dependent kinase.Nature communications · 2026Article
- The D2.B10-DmdThe American journal of pathology · 2026Article
- Extension of Atherosclerosis ApoE-/- Mouse-a Model of Chronic Myocardial Ischemia and Evaluation Method.Journal of cardiovascular translational research · 2026Article
- Carnosine protects human microglia against Aβ oligomers through a multimodal mechanism of action: inhibition of oxidative stress, rescue of cellular energy status, and enhancement of phagocytosis.Frontiers in immunology · 2026Article
- Article
- Promising Role of PKM2 in the Diagnosis and Prognosis of Ovarian Cancer.Anti-cancer agents in medicinal chemistry · 2026Review
- Mitochondrial proteostasis regulated by CRL5Communications biology · 2025Article
- Mapping the complexity of ME/CFS: Evidence for abnormal energy metabolism, altered immune profile, and vascular dysfunction.Cell reports. Medicine · 2025Article
- Methods and Guidelines for Metabolism Studies: Applications to Cancer Research.International journal of molecular sciences · 2025Review
- Acute myeloid leukemia mitochondria hydrolyze ATP to support oxidative metabolism and resist chemotherapy.Science advances · 2025Article
- Placental Adaptation to Hypoxia: The Case of High-Altitude Pregnancies.International journal of environmental research and public health · 2025Review
- VDAC1 inhibitor DIDS uncouples respiration in isolated tissue mitochondria and induces mitochondrial hyperfusion in mammalian cells.BBA advances · 2025Article
- Differential metabolic responses of mouse Leydig and spermatogonia cells to radiofrequency electromagnetic field exposure.Frontiers in public health · 2025Article
- Alteration of mitochondrial function in arthropods during arboviruses infection: a review of the literature.Frontiers in physiology · 2025Review
45 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 2 countries.
Funding
Abstract
Non-proliferating cells generate the bulk of cellular ATP by fully oxidizing respiratory substrates in mitochondria. Respiratory substrates cross the mitochondrial outer membrane through only one channel, the voltage dependent anion channel (VDAC). Once in the matrix, respiratory substrates are oxidized in the tricarboxylic acid cycle to generate mostly NADH that is further oxidized in the respiratory chain to generate a proton motive force comprised mainly of membrane potential (ΔΨ) to synthesize ATP. Mitochondrial ΔΨ then drives the release of ATP(4-) from the matrix in exchange for ADP(3-) in the cytosol via the adenine nucleotide translocator (ANT) located in the mitochondrial inner membrane. Thus, mitochondrial function in non-proliferating cells drives a high cytosolic ATP/ADP ratio, essential to inhibit glycolysis. By contrast, the bioenergetics of the Warburg phenotype of proliferating cells is characterized by enhanced aerobic glycolysis and the suppression of mitochondrial metabolism. Suppressed mitochondrial function leads to lower production of mitochondrial ATP and hence lower cytosolic ATP/ADP ratios that favor enhanced glycolysis. Thus, the cytosolic ATP/ADP ratio is a key feature that determines if cell metabolism is predominantly oxidative or glycolytic. Here, we describe two novel mechanisms to explain the suppression of mitochondrial metabolism in cancer cells: the relative closure of VDAC by free tubulin and the inactivation of ANT. Both mechanisms contribute to low ATP/ADP ratios that activate glycolysis.
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Identifiers
What OpenQuestion holds
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.