Fibronectin antisense oligonucleotide reverses fibrosis in mouse bone marrow models
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Researchers have developed a chemically modified antisense oligonucleotide, FN ASO, designed to silence FN1, the gene encoding fibronectin, as a way to attack the fibrotic bone marrow niche. Systemic delivery of FN ASO in two mouse models of bone marrow fibrosis reduced fibronectin levels and matrix assembly in the marrow, inhibited TGF-beta1-induced activation of mesenchymal stromal cells, and decreased deposition of reticulin fibers and collagen. Transcriptomic analysis in the Jak2V617F-driven model showed downregulation of extracellular matrix, TGF-beta1, and mesenchymal gene programs. Short-term treatment was well tolerated. The findings, posted as a preprint in bioRxiv Cancer Biology on 2026-10-19, suggest fibronectin silencing can remodel the fibrotic marrow microenvironment. Durability of benefit, effects of longer treatment, and translation to patients remain open questions.
Written by a model from the reports · updated 3 hours ago
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- bioRxivPickFibronectin silencing remodels the fibrotic bone marrow niche
Researchers developed a chemically modified antisense oligonucleotide, FN ASO, targeting FN1. Systemic delivery in two mouse models of bone marrow fibrosis reduced fibronectin levels and matrix assembly in the marrow, suppressed TGF-beta1-induced activation of mesenchymal stromal cells, and reduced reticulin fiber and collagen deposition. Transcriptomic analysis in the Jak2V617F-driven model showed downregulation of ECM, TGF-beta1, and mesenchymal gene programs, and short-term treatment was well tolerated.
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