Framework Nucleic Acids Loaded with Quercetin: Protecting Retinal Neurovascular Unit via the Protein Kinase B/Heme Oxygenase-1 Pathway

Retinal neovascular disease is a leading cause of vision loss and blindness globally. It occurs when abnormal new blood vessels form in the retina. In this study, we utilized tetrahedral framework nucleic acids (tFNAs) as vehicles to load quercetin (QUE), a small-molecule flavonoid, forming a deoxyribonucleic acid (DNA) nanocomplex, tFNAs-QUE. Our data show this nanocomplex inhibits pathological neovascularization, reduces the area of retinal nonperfusion area, protects retinal neurons, and preserves the visual function. Further, we discovered that tFNAs-QUE selectively upregulates the AKT/Nrf2/HO-1 signaling pathway, which can suppress pathological vascular growth and exert antioxidative effects. Therefore, this study presents a promising small-molecule-loading mechanism for the treatment of ischemic retinal diseases.

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Publication Details

Journal
ACS Nano
Published
2024-09-13
DOI
https://doi.org/10.1021/acsnano.4c05845
Citations
16
Primary Topic
Retinal Diseases and Treatments
Type
article
Field-Weighted Citation Impact
8.62

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article

Framework Nucleic Acids Loaded with Quercetin: Protecting Retinal Neurovascular Unit via the Protein Kinase B/Heme Oxygenase-1 Pathway

Wenjia Yan, Yunfeng Lin, Xiaoyan Ding, Xiaodi Zhou et al.
16 citations
ACS Nano
Retinal Diseases and Treatments
8.62
article

Framework Nucleic Acids Loaded with Quercetin: Protecting Retinal Neurovascular Unit via the Protein Kinase B/Heme Oxygenase-1 Pathway

Wenjia Yan, Yunfeng Lin, Xiaoyan Ding, Xiaodi Zhou, Qiong Wang, Xiaoxiao Xu, Yili Jin, Li-Mei Chen
article en
16 citations

Abstract

Retinal neovascular disease is a leading cause of vision loss and blindness globally. It occurs when abnormal new blood vessels form in the retina. In this study, we utilized tetrahedral framework nucleic acids (tFNAs) as vehicles to load quercetin (QUE), a small-molecule flavonoid, forming a deoxyribonucleic acid (DNA) nanocomplex, tFNAs-QUE. Our data show this nanocomplex inhibits pathological neovascularization, reduces the area of retinal nonperfusion area, protects retinal neurons, and preserves the visual function. Further, we discovered that tFNAs-QUE selectively upregulates the AKT/Nrf2/HO-1 signaling pathway, which can suppress pathological vascular growth and exert antioxidative effects. Therefore, this study presents a promising small-molecule-loading mechanism for the treatment of ischemic retinal diseases.

ACS NanoVol. 18(38)
Sun Yat-sen University (CN), Shanghai Jiao Tong University (CN), Sichuan University (CN), Stomatology Hospital (CN), Center for Translational Molecular Medicine (NL), State Key Laboratory of Oral Diseases, Zhongshan Ophthalmic Center, Sun Yat-sen University, Chengdu University of Traditional Chinese Medicine (CN)
National Natural Science Foundation of China, Guangzhou Municipal Science and Technology Bureau, Basic and Applied Basic Research Foundation of Guangdong Province
Zero hunger
Openalex Percentile: Top 2%
Retinal Diseases and Treatments
8.62
DOISourceOpenAlex
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