ArticleScience advances2026
Cell surface engineering with a pseudofibrotic ECM reprograms the antifibrotic activity of mesenchymal stromal cells.
Article in Science advances, 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.
- Nanomedicine-based cancer immunotherapy: translational barriers, mechanistic strategies, and future perspectives.Drug delivery · 2026Review
- The role of ECM-PIEZO1-axis-mediated mechanosensation in the central nervous system.Frontiers in neurology · 2026Review
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Authors and funding
11 authors.
Funding
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Abstract
Fibrotic diseases, which impair tissue function and contribute to organ failure, remain a major clinical challenge with limited treatment options. Mesenchymal stromal cells (MSCs) offer promise for antifibrotic therapy via paracrine signaling, but their clinical efficacy is hindered by poor survival and limited functional activity after transplantation. Here, we present a cell surface engineering strategy that reprograms the antifibrotic function of MSCs by constructing a pseudofibrotic extracellular matrix (ECM) on their surface. Through in situ self-assembly of peptide-modified hyaluronic acid, we generate a nanofiber-based matrix that mimics the dense, disordered architecture of fibrotic ECM. This matrix activates the Piezo1/PI3K-Akt signaling pathway, inducing up-regulation of Mmp13-a key collagen-degrading matrix metalloproteinase-in engineered MSCs. In a rat model of myocardial infarction-associated fibrosis, engineered MSCs exhibit robust antifibrotic activity compared to unmodified MSCs. These findings establish a bioinspired strategy for MSC reprogramming and offer a path toward more effective cell-based therapies for fibrotic disease.
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Registered trials
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