The Complex Crosstalk Between Autophagy and ROS Signalling Pathways

The homeostasis between the oxidant and antioxidant levels in cells is altered in several diseases including cancer, neurodegenerative diseases, and inflammatory disorders. Macroautophagy (hereafter referred to as autophagy) is a redox (reduction/oxidation)-sensitive process that results in degradation of cellular constituents such as proteins, lipids, and mitochondria through the lysosomal pathway. There is a complex and mutual relationship between pathways that control levels of reactive oxygen species (ROS) and autophagy. Autophagy is activated by various stimuli in cells and ROS are one of these autophagy inducers. The accumulation of ROS induces autophagy both by direct effect on the core autophagy machinery and by indirect influence on the components of the autophagy-regulatory signaling pathway. In turn, autophagy regulates the abundance of ROS in cells by promoting the clearance of damaged mitochondria and oxidized cellular substrates and by modulating activity of the detoxifying antioxidant systems. ROS are also involved in the initiation of inflammation, a process that required the secretion of several inflammatory mediators. Here, we will discuss the regulation of inflammatory responses by autophagy as a consequence of the interplay of autophagy and ROS signaling pathways.