ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
In Situ Transformable Nanoparticle Effectively Suppresses Bladder Cancer by Damaging Mitochondria and Blocking Mitochondrial Autophagy Flux.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The molecular mechanisms of mitochondrial dynamics and mitophagy and their complex association with cancer drug resistance.Journal of translational medicine · 2025Pooled it
- Topological Quantum Biomaterials Enable Pyroptosis-Senescence Coupling for Enhanced Colorectal Cancer Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Visualized self-propelled nanorobots overcome tumor barriers for boosted photothermal-nanocatalytic synergistic therapy against triple-negative breast cancer.Journal of nanobiotechnology · 2026Article
- Nanomaterial-driven spatiotemporal autophagy modulation: The dual-edged sword in precision cancer therapy.Acta pharmaceutica Sinica. B · 2026Review
- Mitophagy-mediated immune evasion: Shared strategies of pathogens.Redox biology · 2026Review
- Mitophagy in bladder cancer: a double-edged sword in tumor progression and therapy.Journal of translational medicine · 2026Review
- Mitochondria in T‑cell tumor immunity and tumor therapies targeting mitochondria (Review).Oncology reports · 2026Review
- Ferroptosis-autophagy crosstalk in bladder cancer: mechanisms and therapeutic implications.Molecular cancer · 2026Review
- Targeting mitochondrial homeostasis as a cancer treatment strategy: current status and future prospects.Molecular cancer · 2026Review
- Molecular mechanisms of autophagy-lysosomal pathway dysfunction in neurodegenerative diseases and therapeutic strategies for lysosomal repair: a review.Frontiers in neuroscience · 2026Review
- Melatonin Supplementation Relieves Fluoride-Induced Bone Injury via Ion Homeostasis Disorder and PINK1/Parkin-Mediated Mitophagy.Foods (Basel, Switzerland) · 2025Article
- Integrating Metabolic Modulation and Nanomedicine for Cancer Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Identification of biomarkers associated with mitophagy in bladder cancer.Scientific reports · 2025Article
- The Role of N6-Methyladenosine in Mitochondrial Dysfunction and Pathology.International journal of molecular sciences · 2025Review
- In Situ Transformable Nanoparticle Effectively Suppresses Bladder Cancer by Damaging Mitochondria and Blocking Mitochondrial Autophagy Flux.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
14 authors.
Funding
Abstract
Tumor therapeutic strategies based on mitochondrial damage have become an emerging trend. However, the low drug delivery efficiency caused by lysosomal sequestration and the activation of protective mitochondrial autophagy severely restricts the therapeutic efficacy. Herein, an in situ transformable nanoparticle named KCKT is developed to promote lysosomal escape and directly damage mitochondria while blocking mitochondrial autophagy. KCKT exhibits acid responsiveness for precise self-assembly into nanofibers within the lysosomes of cancer cells. The massive accumulation of nanofibers and excessive production of reactive oxygen species (ROS) under sonodynamic therapy synergistically induce lysosomal damage. This facilitates the escape of nanofibers from lysosomal sequestration, thereby enhancing drug delivery. Subsequently, the escaped nanofibers specifically aggregate around the mitochondria for long-term retention and generate ROS under ultrasound irradiation to induce mitochondrial damage. Notably, due to lysosomal dysfunction, damaged mitochondria cannot be cleared by autophagy, further aggravating oxidative damage. These results reveal that KCKT effectively improves drug delivery and mitochondria-targeted therapy efficiency by blocking protective autophagy. These findings hold significant potential for advancing the field of mitochondria-targeted therapy.
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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.