Its possible mechanism is related to the upregulated protective mechanosensing factors (N-CDH and integrin β1) under low-loading hydrostatic pressure (Figure 8), whereas high-magnitude hydrostatic pressure aggravates the breakdown of ECM homeostasis in NP and inner AF via downregulating N-CDH and integrin β1, which attenuated the inhibitory action of YAP/TAZ-mediated cell apoptosis and ECM catabolism. This evidence concerns the gene CHDH and atrial fibrillation.