ArticleNature biomedical engineering2025
A highly mobile adeno-associated virus targeting vascular smooth muscle cells for the treatment of pulmonary arterial hypertension.
Article in Nature biomedical engineering, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Bio-inspired polyphenol-polyelectrolyte WRAP system for geometrically controlled AAV delivery in diverse anatomical sites.Materials today. Bio · 2026Article
- Melk facilitates pulmonary artery smooth muscle cell proliferation and migration in pulmonary hypertension via modulation of YAP/TAZ signaling.Frontiers in cell and developmental biology · 2025Article
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
In pulmonary arterial hypertension (PAH), a phenotypic switch in pulmonary arterial smooth muscle cells (PASMCs) that is primarily caused by aberrant gene regulatory networks can lead to dysregulated vascular remodelling, heart failure or death. No curative therapies for PAH are currently available, presumably because of a lack of viral vectors specifically targeting PASMCs. Here we show that a highly mobile and PASMC-tropic adeno-associated virus variant developed via directed evolution overcomes physical barriers that inhibit its transfer from bronchial airways to vascular layers, ultimately boosting therapeutic efficacy in murine models of PAH. Intratracheal administration of the adeno-associated virus variant carrying a transgene for fibroblast growth factor 12-a key factor regulating the PASMC phenotype-suppressed pulmonary vascular remodelling, prevented the development of PAH in mice and reversed established PAH in rats. The variant's mobility and enhanced tropism for PASMCs may enable curative treatments for PAH.
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Registered trials
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