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. 2023 Jun 5;13(6):e1297. doi: 10.1002/ctm2.1297

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© 2023 The Authors. Clinical and Translational Medicine published by John Wiley & Sons Australia, Ltd on behalf of Shanghai Institute of Clinical Bioinformatics.

This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Graphical abstract. We conducted a single cell transcriptomic analysis to determine chamber‐specific characteristics of the atrial appendages. Potential mechanisms of pathological changes related to atrial fibrillation (AF), including atrial fibrosis through endothelial to mesenchymal transition (EndMT), macrophage polarization and imbalance of local anticoagulation in endocardial endothelial cells (EECs). Disturbed flow during AF‐reprogrammed EECs triggers high a disintegrin and metalloproteinase with thrombospondin motifs 1 (ADAMTS1) expression and decreased tissue factor pathway inhibitor (TFPI) and tissue factor pathway inhibitor 2 (TFPI2), resulting in the prothrombotic state of left atrial appendage (LAA).