ArticleNature communications2019
Mitochondria-specific drug release and reactive oxygen species burst induced by polyprodrug nanoreactors can enhance chemotherapy.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 129 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
129 citing papers in PubMed, 426 citations in OpenAlex.
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- Targeting Highly Reactive Oxygen Species (hROS) for Prodrug Activation through a Cascade Reaction with Kinetic Tunability (CReKT) to Effect Linker Cleavage.Journal of medicinal chemistry · 2026Article
- Silicon quantum dots for neurotheranostic applications in dopamine detection.Journal of nanobiotechnology · 2026Review
- Microenvironment-responsive tetrahedral DNA nanoplatform for specific and enhanced tumor therapy through differential ROS and angiogenesis modulation.Journal of nanobiotechnology · 2026Article
- Black Currant Extract Protects against Oxidative Stress in SH-SY5Y Cells and High-Fat Diet-Induced Cognitive Impairment in C57BL/6 Mice.Journal of microbiology and biotechnology · 2026Article
- Photosensitizing Lipid Nanoparticles for Ferroptosis-Enhanced Photodynamic Cancer Therapy via GPX4 Silencing.Advanced healthcare materials · 2026Article
- Nanomaterial-Mediated Targeting of Mitochondrial Metabolism: Strategies and Applications in Cancer Therapy.International journal of nanomedicine · 2026Review
- Targeting mitochondria for the treatment of neurodegenerative diseases.Frontiers in neuroscience · 2026Review
- The Role of Oxidative Stress and Redox Regulation in Cancer.Cancer treatment and research · 2026Review
- Silibinin Triggers Mitochondrial Apoptosis and Declines Clonogenic Potential in Detroit 562 Human Pharyngeal Carcinoma Cells.Medicina (Kaunas, Lithuania) · 2025Article
- Modified exosomes for targeted delivery of doxorubicin and carvedilol to mitochondria in breast cancer cells.Scientific reports · 2025Article
- Camptothecin in Cancer Therapy: Current Challenges and Emerging Strategies with Nanoemulsions.Pharmaceutics · 2025Review
- Linking mitochondria, fatty acids, and hematopoietic stem cell expansion during infection: implications for aging and metabolic diseases.Stem cells (Dayton, Ohio) · 2025Review
- Review
- A Multifunctional Nanodelivery System Modified by Fusion Peptides Acts as Teriparatide Carrier for Noise-Induced Hearing Loss Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
69 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cells exhibit slightly elevated levels of reactive oxygen species (ROS) compared with normal cells, and approximately 90% of intracellular ROS is produced in mitochondria. In situ mitochondrial ROS amplification is a promising strategy to enhance cancer therapy. Here we report cancer cell and mitochondria dual-targeting polyprodrug nanoreactors (DT-PNs) covalently tethered with a high content of repeating camptothecin (CPT) units, which release initial free CPT in the presence of endogenous mitochondrial ROS (mtROS). The in situ released CPT acts as a cellular respiration inhibitor, inducing mtROS upregulation, thus achieving subsequent self-circulation of CPT release and mtROS burst. This mtROS amplification endows long-term high oxidative stress to induce cancer cell apoptosis. This current strategy of endogenously activated mtROS amplification for enhanced chemodynamic therapy overcomes the short lifespan and action range of ROS, avoids the penetration limitation of exogenous light in photodynamic therapy, and is promising for theranostics.
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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.