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已发表论文
四面体 DNA 纳米结构作为治疗深静脉血栓的多因素纳米治疗平台：靶向坏死性凋亡、氧化应激和炎症
Authors Li Y, Cao W, Lv Y, Yang H, Xu L, Lu Y
Received 14 April 2025
Accepted for publication 21 October 2025
Published 18 November 2025 Volume 2025:20 Pages 13837—13855
DOI https://doi.org/10.2147/IJN.S534411
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Sachin Mali
Yunyan Li,1,* Wenqi Cao,2,* Yixia Lv,3 Hanning Yang,1 Lirong Xu,1 Yongping Lu1
1Department of Ultrasonography, The Affiliated Hospital of Yunnan University, Kunming, Yunnan, People’s Republic of China; 2Graduate school, Kunming Medical University, Kunming, Yunnan, People’s Republic of China; 3Graduate School, Dali University, Dali, Yunnan, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yongping Lu, The Affiliated Hospital of Yunnan University, 176 Qingnian Road, Kunming, Yunnan, 650000, People’s Republic of China, Email luyongpingahynu@126.com
Purpose: Venous thromboembolism (VTE), comprising deep vein thrombosis (DVT) and pulmonary embolism (PE), remains a major clinical challenge due to the limitations of conventional anticoagulant therapies. This study explores tetrahedral DNA nanostructures (TDNs) as a novel therapeutic strategy for DVT by targeting endothelial cell necroptosis and oxidative stress.
Methods: A mouse DVT model was established via inferior vena cava ligation. TDNs were synthesized from four complementary ssDNA strands and validated via gel electrophoresis and atomic force microscopy. Therapeutic effects were assessed through histopathology, Western blot, qPCR, RNA-seq, and oxidative stress markers (SOD/MDA). Mechanistic insights were explored via transcriptomics, co-immunoprecipitation, and bioinformatics.
Results: In a mouse DVT model, TDNs demonstrated remarkable efficacy in mitigating thrombosis, reducing endothelial damage, and restoring vascular homeostasis. Mechanistically, TDNs downregulated the phosphorylation of RIP3 and MLKL, suppressed necroptosis, and modulated inflammatory signaling, specifically via the interaction between PTPRC and CCR9. Transcriptomic analysis confirmed that TDNs ameliorated the dysregulated expression of immune-inflammatory mediators while promoting antioxidative effects by increasing SOD activity and decreasing MDA levels. Bioinformatics and protein interaction assays further unveiled a direct binding between RIP3 and PTPRC, highlighting their roles as molecular targets of TDNs.
Conclusion: These findings underscore TDNs’ potential as a safe and effective nanotherapeutic platform for managing DVT by simultaneously targeting necroptosis, oxidative stress, and inflammation. Future studies are warranted to optimize dosing strategies and evaluate their long-term safety and synergistic use with established anticoagulants.
Keywords: tetrahedral DNA nanostructures, deep vein thrombosis, DVT, necroptosis, oxidative stress, inflammation
1Department of Ultrasonography, The Affiliated Hospital of Yunnan University, Kunming, Yunnan, People’s Republic of China; 2Graduate school, Kunming Medical University, Kunming, Yunnan, People’s Republic of China; 3Graduate School, Dali University, Dali, Yunnan, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yongping Lu, The Affiliated Hospital of Yunnan University, 176 Qingnian Road, Kunming, Yunnan, 650000, People’s Republic of China, Email luyongpingahynu@126.com
Purpose: Venous thromboembolism (VTE), comprising deep vein thrombosis (DVT) and pulmonary embolism (PE), remains a major clinical challenge due to the limitations of conventional anticoagulant therapies. This study explores tetrahedral DNA nanostructures (TDNs) as a novel therapeutic strategy for DVT by targeting endothelial cell necroptosis and oxidative stress.
Methods: A mouse DVT model was established via inferior vena cava ligation. TDNs were synthesized from four complementary ssDNA strands and validated via gel electrophoresis and atomic force microscopy. Therapeutic effects were assessed through histopathology, Western blot, qPCR, RNA-seq, and oxidative stress markers (SOD/MDA). Mechanistic insights were explored via transcriptomics, co-immunoprecipitation, and bioinformatics.
Results: In a mouse DVT model, TDNs demonstrated remarkable efficacy in mitigating thrombosis, reducing endothelial damage, and restoring vascular homeostasis. Mechanistically, TDNs downregulated the phosphorylation of RIP3 and MLKL, suppressed necroptosis, and modulated inflammatory signaling, specifically via the interaction between PTPRC and CCR9. Transcriptomic analysis confirmed that TDNs ameliorated the dysregulated expression of immune-inflammatory mediators while promoting antioxidative effects by increasing SOD activity and decreasing MDA levels. Bioinformatics and protein interaction assays further unveiled a direct binding between RIP3 and PTPRC, highlighting their roles as molecular targets of TDNs.
Conclusion: These findings underscore TDNs’ potential as a safe and effective nanotherapeutic platform for managing DVT by simultaneously targeting necroptosis, oxidative stress, and inflammation. Future studies are warranted to optimize dosing strategies and evaluate their long-term safety and synergistic use with established anticoagulants.
Keywords: tetrahedral DNA nanostructures, deep vein thrombosis, DVT, necroptosis, oxidative stress, inflammation