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Updated: Jul 15, 2026

Long-term Silencing of Intersectin-1s in Mouse Lungs by Repeated Delivery of a Specific siRNA via Cationic Liposomes. Evaluation of Knockdown Effects by Electron Microscopy

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Ligand-Mediated Reprogramming Redirects Liver-Tropic Ionizable Lipid Nanoparticles for Lung-Selective mRNA Delivery.

Zhuxiao Gu^1,2, Xinhong Xiong³, Xiang Chen¹

¹Department of Cardiology, Cardiovascular Disease Center, Institute of Clinical Medicine, Jiangsu Key Laboratory For Cardiovascular Information and Health Engineering Medicine, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, China.

Angewandte Chemie (International Ed. in English)

|July 13, 2026

Summary

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Researchers repurposed liver-targeting lipid nanoparticles (LNPs) for lung-specific messenger RNA (mRNA) delivery. This novel ligand-mediated reprogramming enhances mRNA translation in the lungs, advancing gene therapy applications.

Area of Science:

Biotechnology
Gene Therapy
Nanomedicine

Background:

Lipid nanoparticles (LNPs) are crucial for systemic messenger RNA (mRNA) delivery, but often show liver tropism.
Modifying LNP organ specificity without new chemistry is a significant challenge in gene therapy development.

Purpose of the Study:

To develop a method for reprogramming existing liver-tropic LNPs for targeted mRNA delivery to other organs, specifically the lungs.
To engineer novel lipidoid formulations for enhanced tissue-specific mRNA delivery and therapeutic applications.

Main Methods:

Screened a library of 90 degradable lipidoids to identify a liver-targeting platform (2-t6b).
Engineered reconfigured lipidoids by attaching small molecule ligands to the 2-t6b headgroup for lung targeting.

Keywords:

extrahepatic targeting ionizable lipid lipid nanoparticle mRNA delivery

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Long-term Silencing of Intersectin-1s in Mouse Lungs by Repeated Delivery of a Specific siRNA via Cationic Liposomes. Evaluation of Knockdown Effects by Electron Microscopy

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Utilized proteomics and molecular docking to elucidate the mechanism of enhanced cellular uptake and translation.

Main Results:

Engineered LNPs achieved over 200-fold higher mRNA translation in the lungs compared to parent liver-tropic LNPs.
Identified enhanced binding to vitronectin as a key factor in improved cellular uptake and translation efficiency.
Demonstrated superior efficacy in lung-specific genome editing using ligand-mediated reprogrammed LNPs.

Conclusions:

A modular, ligand-mediated lipid reprogramming strategy can repurpose liver-biased LNPs for lung-selective mRNA delivery.
This approach offers a generalizable framework for developing next-generation tissue-specific mRNA therapies.
Advances in gene editing, protein replacement, and regenerative medicine are facilitated by this targeted delivery system.