Endothelial mechanosensitive transcription factor NR4A1 induced by Piezo1 modulates thrombosis via PTGS2

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ID: 333802
2026
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Abstract
Abstract Endothelial dysfunction-induced platelet activation contributes to thrombosis in major cardiovascular diseases. Endothelial cells sense hemodynamic shear stress via the mechanosensitive ion channel Piezo1, which determines their physiological functions. However, the downstream transcriptional pathways of Piezo1 linking mechanical force to endothelial function remain incompletely defined. Here, nuclear receptor subfamily 4 group A member 1 (NR4A1) is identified as an endothelial mechanosensitive transcription factor induced by Piezo1 that modulates platelet activation and thrombosis. Mechanistically, shear stress is shown to activate Piezo1, resulting in calcium influx and the subsequent activation of protein kinase C δ (PKCδ), which activates extracellular signal-regulated kinase (ERK) to induce NR4A1 transcription. NR4A1 then upregulates prostaglandin-endoperoxide synthase 2 (PTGS2) expression, leading to the increased production of prostacyclin and inhibition of platelet activation and thrombosis. In vivo, mice with endothelial cell-specific deletion of Nr4a1 exhibit greater thrombus weights and faster occlusion. These data establish the Piezo1/Ca2+/PKCδ/ERK/NR4A1/PTGS2 signaling cascade as a critical endothelial mechanotransduction pathway that senses physiological shear force to transcriptionally promote an antithrombotic state.
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openalex_W7223440487 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Xiya Li, Tingting Ye, Sihan Miao, Yixuan Yu, Yuhan Ying, Zhenghua Chen, Xiaoyi Dai, Peng Teng, Yiran Zhang, 徐炎华, Kai Wang, Liang Ma, Qi Zheng, Hai Song
Journal journal of molecular cell biology
Year 2026
DOI
10.1093/jmcb/mjag045
URL
https://doi.org/10.1093/jmcb/mjag045
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