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Abstract Background Enteric infections are among the most common infectious diseases. The aim of this article was to track the global trends in morbidity and mortality from enteric infections in 204 countries or territories from 1990 to 2019. Methods Data were obtained from the Global Burden of Disease 2019 study. Average annual percentage changes (AAPCs) in age-standardized incidence rate (ASIR) and age-standardized mortality rate (ASMR) were calculated to quantify trends in enteric infections. Age-period-cohort models were used to estimate the annual percentage changes from 0 to 4 to 80 − 84 years (local drifts), period and cohort effects between 1990 and 2019 in different socio-demographic index (SDI) regions. Results In 2019, there were 6.59 billion incident cases of enteric infections, and caused 1,748,251 deaths worldwide. From 1990 to 2019, the trend in the global ASIR of enteric infections was relatively stable, but that of ASMR declined (AAPC=-3.30, 95% confidence interval [CI]: -3.54 to -3.07), and global mortality decreased in all age groups. Meanwhile, decreasing trends in ASMR were observed in 173 countries/territories (P

Summary: 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-β1, suggesting that NET1 was involved in the pathological process of cardiac fibrosis. Overexpression of NET1 promoted β-catenin expression in the nucleus and significantly increased the proliferation and migration of cardiac fibroblasts. NET1 may form a complex with β-catenin through GSK3β. Knockdown of β-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 β-catenin, α-SMA, and collagen content induced by MI. In conclusion, NET1 may regulate the activation of Wnt/β-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.