ArticleNanomedicine : nanotechnology, biology, and medicine2017
Cell-penetrating peptide CGKRK mediates efficient and widespread targeting of bladder mucosa following focal injury.
Article in Nanomedicine : nanotechnology, biology, and medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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
4 citing papers in PubMed.
- Nanogels conjugated with cell-penetrating peptide as drug delivery vehicle for treating urinary tract infections.Nanomedicine : nanotechnology, biology, and medicine · 2025Article
- Enhancing the activity of β-lactamase inhibitory protein-II with cell-penetrating peptide against KPC-2-carrying Klebsiella pneumoniae.PloS one · 2024Article
- Strategies to Get Drugs across Bladder Penetrating Barriers for Improving Bladder Cancer Therapy.Pharmaceutics · 2021Review
- Enhanced Anti-Glioma Efficacy by Borneol Combined With CGKRK-Modified Paclitaxel Self-Assembled Redox-Sensitive Nanoparticles.Frontiers in pharmacology · 2020Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
The bladder presents an attractive target for topical drug delivery. The barrier function of the bladder mucosa (urothelium) presents a penetration challenge for small molecules and nanoparticles. We found that focal mechanical injury of the urothelium greatly enhances the binding and penetration of intravesically-administered cell-penetrating peptide CGKRK (Cys-Gly-Lys-Arg-Lys). Notably, the CGKRK bound to the entire urothelium, and the peptide was able to penetrate into the muscular layer. This phenomenon was not dependent on intravesical bleeding and was not caused by an inflammatory response. CGKRK also efficiently penetrated the urothelium after disruption of the mucosa with ethanol, suggesting that loss of barrier function is a prerequisite for widespread binding and penetration. We further demonstrate that the ability of CGKRK to efficiently bind and penetrate the urothelium can be applied toward mucosal targeting of CGKRK-conjugated nanogels to enable efficient and widespread delivery of a model payload (rhodamine) to the bladder mucosa.
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Registered trials
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