ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Tetrahedral DNA Nanostructure-Based Biomimetic Nanovesicles Attenuate Sepsis-Associated ARDS by Suppressing Glycolysis via the BMAL1/PFKFB3 Axis.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Advances in Tetrahedral Framework Nucleic Acids (tFNAs) for Lung Injury Repair: Mechanisms, Therapeutic Applications, and Future Directions.International journal of nanomedicine · 2026Review
- Macrophage metabolic reprogramming in sepsis-associated acute lung injury: mechanisms and therapeutic strategies.Frontiers in immunology · 2026Review
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Authors and funding
24 authors.
Funding
Abstract
Sepsis-associated acute respiratory distress syndrome (SA-ARDS) is a life-threatening complication characterized by excessive pulmonary inflammation and pulmonary edema, lacking effective treatments. This study identifies the transcription factor BMAL1 in alveolar macrophages (AMs) as a key therapeutic target. Mechanistically, BMAL1 represses the expression of the glycolytic enzyme PFKFB3 by binding to the Pfkfb3 promoter, thereby inhibiting glycolysis, M1 polarization of AMs, and the generation of pro-inflammatory cytokines and reactive oxygen species (ROS). Based on this regulatory mechanism, a biomimetic nanoplatform, RM@TNT, is engineered for precise SA-ARDS therapy. Fabricated by hybridizing AM membrane-derived nanovesicles with ROS-responsive liposomes, the nanoplatform encapsulates tetrahedral DNA nanostructures (TNT) preloaded with nobiletin (Nob, a BMAL1 agonist) and Tuftsin (an AM-targeting peptide). Following inhalation, the AM membrane tropism of RM@TNT ensures prolonged pulmonary retention, prompting targeted TNT release within the ROS-rich pathological microenvironment. Tuftsin then precisely delivers TNT to AMs, where Nob is intracellularly released to activate BMAL1. This activation upregulates the BMAL1/PFKFB3 axis, suppressing AM glycolysis, inflammation, and oxidative stress. Treatment with RM@TNT resulted in significantly attenuated lung inflammation, injury, and edema, along with markedly improved survival in SA-ARDS mice. Collectively, this multimodal, targeted metabolic reprogramming approach is a highly promising therapeutic strategy for SA-ARDS.
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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 Socratic graph.