Figure 2.

Schematic representation of the cross talk between endoplasmic reticulum (ER) stress, autophagy and inflammation. Under ER stress conditions, the inflammatory response, which can contribute to cardiovascular disease, is activated by the damaged mitochondria and elevated pro-inflammatory gene expressions. As a feedback, inflammatory response can further enhance ER stress. However, autophagy, which is triggered by ER stress, can inhibit inflammatory response by degrading damaged mitochondrial and inflammation related proteins, which can also further inhibit ER stress. Therefore, ER stress, autophagy, and inflammation are closely related, and one can influence the other.