In our study, we made distinct progress on two aspects: (a) for the first time we observed that in the presence of ET‐1, the suppression of protein levels of water channel AQP1 causes stress fibre collapse, collagen induction, ECM remodelling and contractility alteration of the trabecular meshwork; (b) we identified ATF4 as an ET‐1 sensor in controlling TM remodelling by negatively regulating AQP1 transcription in POAG eyes. The gene discussed is ATF4; the disease is open-angle glaucoma.