Neuroepithelial cell-transforming 1 promotes cardiac fibrosis via the Wnt/8-catenin signaling pathway

This study found that the level of neuroepithelial cell-transforming gene 1 protein (NET1) was significantly increased in a mouse cardiac fibrosis model. Moreover, the expression level of NET1 was increased in cardiac fibrosis induced by TGF-beta 1, suggesting that NET1 was involved in the pathological process of cardiac fibrosis. Overexpression of NET1 promoted beta-catenin expression in the nucleus and significantly increased the proliferation and migration of cardiac fibroblasts. NET1 may form a complex with beta-catenin through GSK3b. Knockdown of beta-catenin alleviated the effects of NET1 overexpression on collagen production and cell migration. In the heart of NET1 knockout mice, NET1 knockout can reduce the expression of beta-catenin, alpha-SMA, and collagen content induced by MI. In conclusion, NET1 may regulate the activation of Wnt/beta-catenin and TGF/Smads signaling pathway, promote collagen synthesis in fibroblasts, and participate in cardiac fibrosis. Thus, NET1 may be a potential therapeutic target in cardiac fibrosis.

Automated summary

This study found that the protein level of NET1 is increased in a mouse cardiac fibrosis model, as well as in cardiac fibrosis induced by TGF-beta 1. Overexpression of NET1 promotes beta-catenin expression and increases the proliferation and migration of cardiac fibroblasts. NET1 may interact with beta-catenin through GSK3b. Knockdown of beta-catenin alleviates the effects of NET1 overexpression on collagen production and cell migration. In conclusion, NET1 may regulate the activation of Wnt/beta-catenin and TGF/Smads signaling pathway, promote collagen synthesis in fibroblasts, and participate in cardiac fibrosis.