ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Fibroblast Activation Protein Promotes Thoracic Aortic Dissection via PLAUR/ITGB1-Mediated Pro-inflammatory Macrophage Polarization.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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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Who cites it
2 citing papers in PubMed.
- Unraveling the roles of fibroblast activation protein‑positive cancer‑associated fibroblasts in cancer: From mechanisms to therapy (Review).International journal of oncology · 2026Review
- Integrated clinical and multi-omics analysis links composite inflammatory indices to macrophage-associated molecular programs in aortic dissection.Frontiers in genetics · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
backgroundThoracic aortic dissection (TAD) is a lethal vascular emergency lacking targeted therapies. Fibroblast activation protein (FAP), a protease implicated in tissue remodeling, exhibits unknown roles in TAD pathogenesis.
methodsHuman TAD specimens and β-aminopropionitrile-induced TAD models were used to assess FAP expression. Global and fibroblast-specific Fap knockout mice were generated to evaluate biological effects of FAP. Bulk and single-cell RNA sequencing were used to map cellular crosstalk and dysregulated signaling pathways. A combination of pharmacological inhibition (Ac-Gly-BoroPro), surface plasmon resonance (SPR), co-immunoprecipitation (co-IP), and functional rescue experiments was utilized to dissect the enzymatic versus nonenzymatic functions of FAP and its interaction with PLAUR/ITGB1 signaling.
resultsFibroblast-derived FAP was significantly upregulated in TAD lesions. Fap deletion markedly attenuated inflammatory infiltration, extracellular matrix degradation, and TAD incidence. Surprisingly, pharmacological inhibition of FAP's enzymatic activity failed to protect against TAD. SPR, co-IP, and functional assays revealed that FAP binds directly to macrophage PLAUR via nonenzymatic sites. This interaction triggers ITGB1/FAK signaling, promoting a pro-inflammatory macrophage phenotype that drives TAD progression.
conclusionThis study demonstrates that FAP promotes TAD through a nonenzymatic mechanism involving fibroblast-macrophage crosstalk via the FAP/PLAUR/ITGB1/FAK axis. Targeting this pathway might offer a promising therapeutic strategy for TAD.
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