Fig. 11

Simplified model illustrating how the overexpression of PADI2 could induce endoplasmic reticulum (ER) stress and autophagy. When PADI2 is activated or overexpressed, citrullination and accumulation of cellular proteins occur, resulting in ER stress and induces UPR signaling via activation of the PERK/eIF2α pathway, as well as the production of ROS to induce autophagy. Additionally, PADI2 stimulates the activation of Th17-like T cells and the production of pro-inflammatory cytokines such as IL-6, IL-17, IL-21, and IL-22, ultimately resulting in the ACAD