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This study untangles the mechanism by which epicardial cells, serving as critical mechanosensors, mediate fibrosis through interactions with fibroblasts. Epicardial cells mediate fibroblast activation via the Chemerin-Cmklr1 paracrine signaling pathway through the Pi3k-Akt1-Pou3f1 axis. Breaking Chemerin-Cmklr1 axis by α-NETA demonstrated significant therapeutic potential, supporting its potential clinical translation.

本研究厘清了作为关键机械感受器的心外膜细胞（epicardial cells）通过与成纤维细胞（fibroblasts）相互作用介导纤维化的具体机制。心外膜细胞可通过Pi3k-Akt1-Pou3f1信号轴，经由趋化素-Cmklr1（Chemerin-Cmklr1）旁分泌信号通路介导成纤维细胞活化。采用α-NETA阻断趋化素-Cmklr1轴可展现出显著的治疗潜力，为其临床转化提供了有力支撑。