ArticleVirology journal2023
Reactive oxygen species enhance rAAV transduction by promoting its escape from late endosomes.
Article in Virology journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Engineering challenges and translational opportunities in emerging gene delivery platforms.Nature biomedical engineering · 2026Review
- Impact of Nanoparticle Stiffness on Endosomal Escape and Signaling Pathways in Cytosolic Delivery.Advanced healthcare materials · 2025Article
- Navigating the Hurdles of Intra-Articular AAV Gene Therapy.International journal of molecular sciences · 2025Review
- Effective Reduction of Transgene-Specific Immune Response With rAAV Vectors Co-Expressing miRNA-UL112-5p or ERAP1 shRNA.Journal of cellular and molecular medicine · 2025Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRecent seminal studies have revealed that endosomal reactive oxygen species (ROS) promote rather than inhibit viral infection. Some ROS generators, including shikonin and H
methodsTo understand the effects of ROS on the transduction of rAAV vectors, especially the rAAV subcellular distribution profiles, this study systematically explored the effect of ROS on each step of rAAV intracellular trafficking pathway using fluorescently-labeled rAAV and qPCR quantification determination.
resultsThe results showed promoted in-vivo and in-vitro rAAV transduction by ROS exposure, regardless of vector serotype or cell type. ROS treatment directed rAAV intracellular trafficking towards a more productive pathway by upregulating the expression of cathepsins B and L, accelerating the rAAV transit in late endosomes, and increasing the rAAV nucleus entry.
conclusionsThese data support that ROS generative drugs, such as shikonin, have the potential to promote rAAV vector transduction by promoting rAAV's escape from late endosomes, and enhancing its productive trafficking to the nucleus.
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Registered trials
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