ReviewNature reviews. Drug discovery2010
Targeting mitochondria for cancer therapy.
Review in Nature reviews. Drug discovery, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 599 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
599 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Natural Compounds for the Treatment of Cutaneous Squamous Cell Carcinoma: A Systematic Review.International journal of molecular sciences · 2026Pooled it
- In vitro cytotoxic and apoptotic effects of chitosan-coated gold nanoparticles on HT-29 human colorectal adenocarcinoma cells.BMC gastroenterology · 2026Article
- Spotlight on cGAS-STING: role in disease pathogenesis and therapeutic potential.Molecular biomedicine · 2026Review
- An Exploratory LC-HRMS Metabolomics Study of Culture Medium-Dependent Metabolic Variation and Bioactivity in Ten Fungal Strains.International journal of molecular sciences · 2026Article
- Network-Guided Identification of Plant-Derived Modulators of Stress-Adaptive Signalling in Neuroblastoma.International journal of molecular sciences · 2026Article
- Suppression of mitochondrial energy production by a photosynthetic bacterial cupredoxin peptide inhibits tumor growth.Signal transduction and targeted therapy · 2026Article
- Genistein and Butein as Bioactive Polyphenols: Molecular Targets, Metabolic Regulation, and Mechanistic Insights.Life (Basel, Switzerland) · 2026Review
- Article
- Single-Mitochondrion ATP Profiling Directs Discovery of Targetable OXPHOS Dependency in Cancers.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Roburic Acid as a Therapeutic Candidate: Antiproliferative Activity and Secondary Cell Death Response in Colorectal Cancer Cells.International journal of molecular sciences · 2026Article
- A Novel Wogonin Derivative Induces Apoptosis in PC-3M Cells by Targeting Mitochondrial Dysfunction and Activating the ROS-p38/MAPK Pathway.Molecules (Basel, Switzerland) · 2026Article
- 5-Aminolevulinic Acid-Based Radiodynamic Therapy for Malignant Gliomas: A Conceptual Framework for Mitochondria-Centered Mechanisms, Target Cell States and Translational Perspectives.Life (Basel, Switzerland) · 2026Review
- Bioactive glass nanoparticles induce intrinsic p53-dependent apoptosis and promote genomic instability via ROS overproduction and mitochondrial depolarization in triple-negative breast cancer cells.Scientific reports · 2026Article
- Nano-Engineered Delivery of the Pro-Apoptotic KLA Peptide: Strategies, Synergies, and Future Directions.Biomolecules · 2026Review
- Triple-Targeted DNA Nanozyme Executes Disulfidptosis for Glioma Elimination.Theranostics · 2026Article
- Overcoming resistance in lung cancer: combined mitochondrial destabilization by lipophilic cations and doxycycline in hypoxic non-small cell lung carcinoma.Frontiers in pharmacology · 2026Article
- Metabolomics-guided identification of bioactive phytometabolites from South African plants targeting neuroblastoma.Experimental biology and medicine (Maywood, N.J.) · 2026Article
- Mitochondrial Dysfunction as a Targetable Vulnerability in Gastric Cancer: From Carcinogenesis to Apoptosis (A Narrative Review).Journal of Cancer · 2026Review
- Synergistic targeting of cancer cells through simultaneous inhibition of key metabolic enzymes.Cell death and differentiation · 2025Article
- Induction of potent preferential cell death, severe DNA damage and p53-independent ROS-mediated mitochondrial apoptosis by CaTiONaunyn-Schmiedeberg's archives of pharmacology · 2025Article
539 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria are the cells' powerhouse, but also their suicidal weapon store. Dozens of lethal signal transduction pathways converge on mitochondria to cause the permeabilization of the mitochondrial outer membrane, leading to the cytosolic release of pro-apoptotic proteins and to the impairment of the bioenergetic functions of mitochondria. The mitochondrial metabolism of cancer cells is deregulated owing to the use of glycolytic intermediates, which are normally destined for oxidative phosphorylation, in anabolic reactions. Activation of the cell death machinery in cancer cells by inhibiting tumour-specific alterations of the mitochondrial metabolism or by stimulating mitochondrial membrane permeabilization could therefore be promising therapeutic approaches.
Indexed as
Identifiers
20467424What 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.