Fig. 8: A summary of the results of the present study. | Cell Death & Disease

Fig. 8: A summary of the results of the present study.

From: Autophagy caused by oxidative stress promotes TGF-β1-induced epithelial-to-mesenchymal transition in human peritoneal mesothelial cells

Fig. 8

In HPMCs, TGF-β1-induced NOX4 activation resulted in increased reactive oxygen species (ROS) generation, leading to mitochondrial damage. Increased ROS within the mitochondria activates the PI3K/Akt pathway, induces mitochondrial damage, and promotes the activation of autophagy. Autophagy activation promotes epithelial-to-mesenchymal transition (EMT) in HPMCs via the Smad2/3, PI3K/Akt, and ERK/P38 pathways. Both direct inhibition of autophagy by 3-MA or ATG5 gene silencing, and indirect inhibition of autophagy through NOX4 inhibition by GKT137831, ameliorated the TGF-β1-induced EMT in HPMCs. Upregulation is shown in red and downregulation in blue.

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