ArticleiScience2025
Fibrinogen triggers perivascular fibroblast activation in a mouse model of cortical ischemic stroke.
Article in iScience, 2025. 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.
- Unwinding the Neurovascular Unit: The Vascular Extracellular Matrix and Mechanochemical Collagen Functionalization in Vascular Dementia.International journal of molecular sciences · 2026Review
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Authors and funding
9 authors.
Funding
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Abstract
Fibrotic scar formation caused by stromal cells is often associated with chronic, non-healing pathology impeding repair of the central nervous system (CNS). Perivascular fibroblasts (PVFs) in the perivascular space are activated, express and deposit excess collagen I (Col I), and form a fibrotic scar following CNS disease. Here we show that blood-derived fibrinogen deposition in the perivascular space following photothrombosis, a mouse model for ischemic stroke, initially induces PVF activation. Pharmacological fibrinogen depletion reduces PVF activation and migration away from blood vessels to build up the fibrotic scar. Fibrinogen-induced beta1 integrin signaling in PVF regulates Col I expression. Single-cell RNA sequencing and genetic approches revealed a contribution of fibrinogen-induced myeloid cells to PVF activation. Fibrinogen depletion abrogates PVF-astrocyte signaling and lesion border formation, promoting neuronal survival and plasticity. We propose that fibrinogen is a critical trigger for fibrotic scar formation, inhibiting neuronal regeneration after stroke.
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