ArticleAdvanced materials (Deerfield Beach, Fla.)2026
Ultrasound-Responsive Dual-Prodrug Nanoassembly for "Fenestrae-Restoration Strategy" in Liver Fibrosis Therapy.
Article in Advanced materials (Deerfield Beach, Fla.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Liver sinusoidal endothelial cell fenestrations in metabolic liver disease: from molecular mechanisms to therapeutic perspectives.Cell communication and signaling : CCS · 2026Review
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Authors and funding
9 authors.
Funding
Abstract
Liver fibrosis is a serious yet reversible intermediate stage in the progression of liver disease, which can ultimately advance to cirrhosis and hepatocellular carcinoma. Targeted and selective inhibition of activated hepatic stellate cells (aHSCs) has emerged as a promising therapeutic strategy for the treatment of liver fibrosis. However, the capillarization of liver sinusoidal endothelial cells (LSECs) characterized by the loss of fenestrae and continuous formation of basement membrane presents a significant barrier to effective delivery of anti-fibrotic agents. In this study, we propose a novel "fenestrae-restoration strategy" employing ultrasound-responsive polymeric dual prodrug nanoassembly (PMS) co-loaded with nitric oxide prodrug (mSNO) and poly-metformin (PMet). PMS is engineered for controllable, ultrasound-triggered release of nitric oxide from mSNO, which activates soluble guanylate cyclase. This results in upregulation of intracellular cyclic guanosine monophosphate that facilitates the reversal of LSECs capillarization, restoring fenestrae and enhancing endothelial permeability. This restoration enables PMS to traverse the hepatic sinusoidal barrier, followed by accumulation in fibrotic tissue, where PMet is internalized by aHSCs. In lysosomes, metformin released from PMet ultimately inhibits aHSCs proliferation and migration via the AMPK-mTOR pathway deregulation. The therapeutic efficacy and underlying mechanisms of "fenestrae-restoring strategy" were comprehensively validated in preclinical CCl
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